Tokushima University / Educator and Researcher Directory --- Takeda, Eiji

Personal Web Page

https://researchmap.jp/read0017336 (researchmap)

Field of Study

○	Pathological Nutrition, Bone Metabolism and Endocrinology, Pediatrics

Subject of Study

○	カルシウム·リン·ビタミンD代謝調節機序の解明と骨健康増進に関する研究, 食品機能解析と機能性食品開発に関する研究, 栄養素の転送と代謝障害に関する研究, 食品によるストレス制御に関する研究, 生活習慣病，肝障害·癌·糖尿病·外科手術患者等の栄養療法に関する研究 (臨床栄養管理, 機能性食品, 遺伝子発現調節, ストレス制御, リン代謝調節)

Book / Paper

Book:

1.	Masashi Masuda, Hironori Yamamoto, 竹井悠一郎, 中橋乙起, 足立雄一郎, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Hiroshi Sakaue, 宮崎淳, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b), The Vitamin Society of Japan, Nov. 2020. (Summary) ビタミン欠乏(VAD)ラットにall-transレチノイン酸(ATRA)を投与後，腸管のNpt2b発現を中心としたリン吸収への影響と，ラットNpt2b遺伝子プロモーターを用いたATRAによるNpt2b生化学転写調節機構について検討した．VADラットにATRAを腹腔内投与した18時間後，血漿リン濃度はビタミンAによる影響を認めなかったが，腸管リン酸取り込み活性，Npt2b蛋白発現量およびmRNA発現量はATRA投与により抑制された．マウス胎児線維芽細胞株NIH3T3細胞を用いたルシフェラーゼアッセイの結果，レチノイン酸受容体(RAR)/レチノイドX受容体存在下においてATRAおよびRARアゴニスト濃度依存的にNpt2b遺伝子プロモーター活性は低下した．デリーションアッセイの結果，ATRAによるNpt2b遺伝子プロモーター活性の低下は，転写因子CCAAT/enhancer-binding protein(C/EBP)依存的であることが示唆された． (Keyword) all-trans retinoic acid (ATRA) / retinoic acid receptor (RAR) / CCAAT/enhancer-binding protein (C/EBP) / small intestine / type II sodium-dependent phosphate co-transporter (Npt2b) (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.94.11_545 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390571704642711680 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.94.11_545 (DOI: 10.20632/vso.94.11_545, CiNii: 1390571704642711680)
2.	Eiji Takeda, Yoshiko Suzuki, Akiko Matsumura, Yutaka Nakaya, Rie Tsutsumi, Hiroshi Sakaue, Yasuhiro Hamada, Akiko Hata and 他42人 : Guidebook of Nutrition Support Team 2017, 5th Edition, Jul. 2017.
3.	Eiji Takeda, Hisami Okumura, 中尾真理 and Yutaka Taketani : 抗ストレス効果を示す食品・食生活とバイオマーカー, CMC Publishing Co.,Ltd., Sep. 2013.
4.	Hidekazu Arai, Hiroshi Sakaue, Eiji Takeda, Yutaka Taketani, 藤岡由夫 and 細川雅也 : 臨床病態栄養学第3版, 文光堂, Sep. 2013.
5.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : Complications and Managements of Hyperphosphatemia in Dialysis, InTech, Nov. 2011.
6.	Eiji Takeda : NSTガイドブック2011改訂第3版, Medical Review Co.,Ltd, Osaka, Jan. 2011.
7.	Eiji Takeda : がん栄養療法ガイドブック第2版, Medical Review Co.,Ltd, Osaka, Jan. 2011.
8.	Eiji Takeda : 最新呼吸リハビリテーション, Nankodo, Tokyo, Oct. 2010.
9.	Eiji Takeda : 最新育児小児病学改訂第6版, Nankodo, Tokyo, Sep. 2010.
10.	Eiji Takeda : 静脈・経腸栄養(第3版)ー基礎・臨床研究のアップデートー, NIPPONRINSHOSHA Co.,Ltd., Osaka, Mar. 2010.
11.	Eiji Takeda : 今日の診断指針第6版, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2010.
12.	Eiji Takeda : コメディカルのための論文の書き方の基礎知識, Medical Review Co.,Ltd, Osaka, Jan. 2010.
13.	川浦昭彦谷田憲俊泉啓介秋山純一水谷雅年野中紘士 and Eiji Takeda : Inhibition of angiogenesis as a mechanism for inhibitory effect of 1-hydroxyvitamin D3 on N- methyl-N`- nitro N - nitrosoguanidine - induced gastrointestinal carcinogenesis in Wistar rats, Mar. 2009.
14.	Eiji Takeda : 小児の栄養, Mar. 2009.
15.	Eiji Takeda : 1.1.臨床栄養学・臨床栄養学の意義/1.2.臨床栄養学・栄養素の代謝と機能/1.4.臨床栄養学・栄養必要量/4.1.代謝性疾患・肥満とメタボリックシンドローム/4.6.代謝性疾患・先天性代謝異常, Mar. 2009.
16.	Eiji Takeda and Hironori Yamamoto : 1.栄養素の役割a.3大栄養素の消化吸収，b.糖質の役割，c.脂肪の役割，d.蛋白質の役割，e.ビタミンの役割，f.微量元素の役割，g.水の役割，h.ミネラルの役割, Jan. 2009.
17.	Eiji Takeda : 特集医師に必要な臨床栄養学栄養素の過不足による疾患, Nov. 2008.
18.	Eiji Takeda and Hisami Okumura : 食品技術総合事典, Jun. 2008.
19.	Eiji Takeda : 小児における栄養投与量の決定,注意点, May 2008.
20.	Eiji Takeda : 第1章日本病態栄養学会の高度専門職業人認定とチーム医療栄養管理の高度専門職業人の役割と責任, Apr. 2008.
21.	Eiji Takeda : 骨吸収と骨形成のカップリング, 2008.
22.	Hisami Okumura, 廣瀬美和 and Eiji Takeda : ビタミンK高含有経腸栄養剤のワルファリン療法に及ぼす影響, 2008.
23.	Eiji Takeda : ビタミン異常症(欠乏症/過剰症), 2008.
24.	Eiji Takeda, 阿望幾久子 and 上番増喬 : メタボリックシンドローム, 2008.
25.	Eiji Takeda : 第3章4-F 先天性代謝異常症，最新栄養予防・治療学, Nagai Shoten Co., Tokyo, Jan. 2007.
26.	Eiji Takeda and Yutaka Taketani : 第1章2-C ストレスと栄養，最新栄養予防・治療学, Nagai Shoten Co., Tokyo, Jan. 2007.
27.	Eiji Takeda, Toshiya Okahisa, Yasuko Takahashi, 国清紀子, Akiko Matsumura, Yutaka Nakaya, Masaharu Nishi, Yutaka Taketani, Katsuhiko Yoshimoto, Junji Terao, 美馬福恵, Masami Yoshioka, 山田静恵, Keisuke Ishizawa, 鈴木麗子, chiyo Fujita, Hidekazu Arai, Masashi Kuwahata and Kazuko Okada : 栄養管理のチーム医療, 文光堂, Tokyo, Apr. 2006.
28.	Yutaka Nakaya, Masashi Kuwahata, Akira Tangoku, Toshio Doi, Yutaka Taketani, Yoshihiko Noma, Eiji Takeda, Hiroyuki Azuma, Mitsuo Shimada, Nobuhiro Kurita, Tetsuro Ohmori, Masaharu Nishi, Yoshinori Aono, Yasuhiko Nishioka, Katsuhiko Yoshimoto and ほか 65名 : NST用語ハンドブック, Medical Review Co.,Ltd, Tokyo, Feb. 2006.
29.	Eiji Takeda : 改訂版認定病態栄養専門師のための病態栄養ガイドブック, Medical Review Co.,Ltd, Osaka, Apr. 2005.
30.	Eiji Takeda : 第4回「栄養とエイジング」国際会議ヘルスプロモーションの科学, KENPAKUSHA, Tokyo, Apr. 2005.
31.	Eiji Takeda : 臨床栄養学, 文光堂, Apr. 2004.
32.	Eiji Takeda : 臨床医科学入門, 株式会社光生館, Tokyo, Apr. 2004.
33.	Eiji Takeda : Kyo, 日本新薬株式会社, Kyoto, Mar. 2004.
34.	Eiji Takeda : 栄養科学シリーズNEXT 臨床医学入門, Kodansha, Tokyo, Dec. 2003.
35.	Eiji Takeda, 中屋豊 and 高橋保子 : 栄養士，医療スタッフのための実践臨床栄養学メモ第2版, 文光堂, Tokyo, Nov. 2003.
36.	Eiji Takeda : ビタミン代謝異常, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2003.
37.	Eiji Takeda, 高橋保子 and Yutaka Nakaya : 栄養士，医療スタッフのための実践臨床栄養学メモ，改訂2版, 文光堂, Tokyo, 2003.
38.	庄司有里, Hidekazu Arai, Akira Mizuno, 佐々木一, 水本憲司, 有馬裕史, 松浦基, 粟根尚美, Yutaka Taketani, Toshio Doi and Eiji Takeda : 新規流動食(MHN-01)および従来流動食(SBF)の食後血糖値およびインスリン分泌量の比較, Japan Society of Metabolism and Clinical Nutrition, 2003.
39.	Eiji Takeda, Hisami Okumura and Hidekazu Arai : 看護のための最新医学講座, Nakayama-Shoten Co., Ltd., Tokyo, Jul. 2002.
40.	Eiji Takeda, 渡邊孟 and 奥田拓道 : 高齢者の食と栄養管理, KENPAKUSHA, Tokyo, May 2001. (Keyword) 高齢者の食と栄養管理に関する対策と提言
41.	Eiji Takeda and 高橋保子 : 栄養士，医療スタッフのための実践臨床栄養学メモ, 文光堂, Tokyo, Nov. 2000. (Keyword) 病態の理解と把握 / 栄養アセスメント / 栄養摂取法と補給法 / 栄養管理法 / カルテと症例のまとめ方
42.	Eiji Takeda and 中坊幸弘 : 臨床栄養学, 株式会社講談社サイエンティフィク, Tokyo, Oct. 1998. (Keyword) 臨床栄養学の意義 / 栄養素の代謝と機能 / 栄養所要量 / obesity / 先天性代謝異常症
43.	Eiji Takeda, 山下亀次郎 and 清野裕 : 医師，管理栄養士のための栄養代謝テキスト, 文光堂, Tokyo, Nov. 1997. (Keyword) energy metabolism / 骨粗鬆症 / 肝疾患 / 栄養不良 / ビタミン

Academic Paper (Judged Full Paper):

1.	Yuya Ikezumi, Yasushi Matsuura, Teruhiro Morishita, Noriko Ide, Isao Kitada, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue, Yutaka Taketani, Koichi Sairyo and Eiji Takeda : Necessity of daily 1000-IU vitamin D supplementation for maintaining a sufficient vitamin D status., The Journal of Medical Investigation : JMI, Vol.69, No.1.2, 135-140, 2022. (Summary) The changes in the serum 25-hydroxyvitamin D (25(OH)D) concentrations after daily 1000-IU vitamin D intake for 3 months (3-month-VD), 6 months (6-month-VD) and then 6-month cessation of vitamin D in-take (6-month-VD cessation) were examined. The serum 25(OH)D levels in 11 male and 16 female subjects were 12.1±3.5 ng/mL at baseline, increased to 27.1±4.7 ng/mL at 3-month-VD, 28.5±5.1 ng/mL at 6-month-VD and decreased to 16.4±4.0 ng/mL at 6-month-VD cessation. The present study suggested that a vitamin D intake of 1000 IU/day is required to maintain the 25(OH) D concentration at 30 ng/mL or higher without vitamin D intoxication. J. Med. Invest. 69 : 135-140, February, 2022. (Keyword) Dietary Supplements / female / Humans / male / Nutritional Status / vitamin D / Vitamin D Deficiency / Vitamins (Tokushima University Institutional Repository) ● Metadata: 117024 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.135 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466135 ● Search Scopus @ Elsevier (PMID): 35466135 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.135 (Tokushima University Institutional Repository: 117024, DOI: 10.2152/jmi.69.135, PubMed: 35466135)
2.	Teruhiro Morishita, Michiko Sato, Takafumi Katayama, Nami Sumida, Hiroshi Omae, Shigeko Satomura, Masae Sakuma, Hidekazu Arai, Akihiko Kawaura, Eiji Takeda, Shinsuke Katoh and Koichi Sairyo : Cut-off values for skeletal muscle strength and physical functions in Japanese elderly with walking difficulty., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 48-52, 2021. (Summary) Age-related changes in muscle strength and physical functions, and the association between vitamin D status and skeletal muscle functions were investigated in 36 men (21-90 years old) and 52 women (21-104 years old). Significant ageing-related decreases in several skeletal muscle functions and serum 25-hydroxyvitamin D [25(OH)D] levels were observed in both men and women. Cut-off values for the Timed up and go (TUG) test, walking speed, handgrip strength and Barthel Index (BI) detecting walking difficulties in the receiver operating characteristic (ROC) analysis were 11.1 sec, 0.60 m / sec, 17.0 kg, and 90.0 in males, and 28.6 sec, 0.43 m / sec, 13.9 kg, and 67.5 in females, respectively. By comparing personal present data of muscle strength with these cut-off values, people can easily understand their process to walking difficulty. Therefore, these results are important and useful to avoid or to delay a handicapped and dependent status by improving the vitamin D level, rehabilitation and nursing care. J. Med. Invest. 68 : 48-52, February, 2021. (Tokushima University Institutional Repository) ● Metadata: 115984 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.48 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994479 ● Search Scopus @ Elsevier (PMID): 33994479 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.48 (Tokushima University Institutional Repository: 115984, DOI: 10.2152/jmi.68.48, PubMed: 33994479)
3.	Yasushi Matsuura, Teruhiro Morishita, Michiko Sato, Nami Sumida, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue, Yutaka Taketani, Koichi Sairyo, Akihiko Kawaura and Eiji Takeda : Effects of daily 1,000-IU vitamin D-fortified milk intake on skeletal muscle mass, power, physical function and nutrition status in Japanese., The Journal of Medical Investigation : JMI, Vol.68, No.3.4, 249-255, 2021. (Summary) An intervention study was conducted to investigate the effects of daily 1,000-IU vitamin D-fortified milk intake on skeletal muscle mass, power, physical function and nutrition status in 26 healthy people and 8 older adults living in a nursing home. The serum 25-hydroxyvitamin D [25(OH)D] level was 13.4 ± 0.8 ng / mL and it markedly increased to 29.6 ± 0.9 ng / mL after daily 1000-IU vitamin D-fortified milk intake for 6 months. Handgrip strength (kg) also significantly increased in the 21-50 years and total groups, and male subjects, and the timed up and go test signiﬁcantly improved in the 21-50 years and total groups, and female subjects after 6-month vitamin D intake. However, there were no significant differences between baseline and post-treatment in the Barthel Index (BI), walking speed (m / sec) or skeletal muscle mass (kg, % of BW, kg / m2). Therefore, the present study suggested that vitamin D-fortified milk intake is effective at improving muscle strength and physical function in Japanese, although further studies are needed, particularly for older adults. J. Med. Invest. 68 : 249-255, August, 2021. (Keyword) Aged / Animals / female / Hand Strength / Humans / Japan / male / Milk / Muscle Strength / Muscle, Skeletal / Nutritional Status / Postural Balance / Time and Motion Studies / vitamin D (Tokushima University Institutional Repository) ● Metadata: 116490 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.249 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34759139 ● Search Scopus @ Elsevier (PMID): 34759139 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.249 (Tokushima University Institutional Repository: 116490, DOI: 10.2152/jmi.68.249, PubMed: 34759139)
4.	Yoko Narasaki, Michiyo Yamasaki, Sayaka Matsuura, Mayumi Morinishi, Tomomi Nakagawa, Mami Matsuno, Misaki Katsumoto, Sachi Nii, Yuka Fushitani, Kohei Sugihara, Tsuneyuki Noda, Takeshi Yoneda, Masashi Masuda, Hisami Okumura, Eiji Takeda, Hiroshi Sakaue, Hironori Yamamoto and Yutaka Taketani : Phosphatemic Index Is a Novel Evaluation Tool for Dietary Phosphorus Load: A Whole-Foods Approach., Journal of Renal Nutrition, Vol.30, No.6, 493-502, 2020. (Tokushima University Institutional Repository) ● Metadata: 114726 (Link to Publication Site) ● Publication site (DOI): 10.1053/j.jrn.2020.02.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32778471 ● Search Scopus @ Elsevier (PMID): 32778471 ● Search Scopus @ Elsevier (DOI): 10.1053/j.jrn.2020.02.005 (Tokushima University Institutional Repository: 114726, DOI: 10.1053/j.jrn.2020.02.005, PubMed: 32778471)
5.	Masashi Masuda, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Yamanaka-Okumura, Hiroshi Sakaue, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b)., The Biochemical Journal, Vol.477, No.4, 817-831, 2020. (Summary) Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Although we previously reported that vitamin A-deficient (VAD) rats had increased urine Pi excretion through the decreased renal expression of Npt2a and Npt2c, the effect of vitamin A on the intestinal Npt2b expression remains unclear. In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. The transcriptional activity of reporter plasmid containing the promoter region of the rat Npt2b gene was reduced by ATRA in NIH3T3 cells overexpressing retinoic acid receptor (RAR) and retinoid X receptor (RXR). On the other hand, CCAAT/enhancer-binding proteins (C/EBP) induced transcriptional activity of the Npt2b gene. Knockdown of the C/EBP gene and a mutation analysis of the C/EBP responsible element in the Npt2b gene promoter indicated that C/EBP plays a pivotal role in the regulation of Npt2b gene transcriptional activity by ATRA. EMSA revealed that the RAR/RXR complex inhibits binding of C/EBP to Npt2b gene promoter. Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene. (Tokushima University Institutional Repository) ● Metadata: 114417 (Link to Publication Site) ● Publication site (DOI): 10.1042/BCJ20190716 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357 ● Search Scopus @ Elsevier (PMID): 32016357 ● Search Scopus @ Elsevier (DOI): 10.1042/BCJ20190716 (Tokushima University Institutional Repository: 114417, DOI: 10.1042/BCJ20190716, PubMed: 32016357)
6.	Michiko Sato, Teruhiro Morishita, Takafumi Katayama, Shigeko Satomura, Hiroko Okuno, Nami Sumida, Masae Sakuma, Hidekazu Arai, Shinsuke Katoh, Koichi Sairyo, Akihiko Kawaura and Eiji Takeda : Relationship between age-related decreases in serum 25-hydroxyvitamin D levels and skeletal muscle mass in Japanese women., The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 151-157, 2020. (Summary) A clearer understanding of skeletal muscle mass (SMM) in middle-aged and elderly individuals is important for maintaining functionality. In the present study, age-related changes in SMM, the threshold of SMM with walking difficulty, intestinal nutrient absorption rate, and various serum factors were examined in Japanese populations of different ages. We used 24-h creatinine excretion as a measure of total body SMM. Age-related decreases in SMM, intestinal nutrient absorption rates, and serum 25-hydroxyvitamin D [25(OH)D] concentrations were significantly higher in women than in men. The cut-off values for SMM (kg), its percentage of total body weight (BW), the SMM index [SMMI] (Kg / m2), and creatinine height index (CHI) (%) in elderly individuals with walking difficulty were approximately 8-10 kg, 17-20% of BW, 3.9-4.6 kg / m2, and 44%, respectively. Serum 25(OH)D concentrations were closely associated with SMM (kg, % of BW, kg / m2) and CHI (%) as well as the intestinal absorption rates of nitrogen (%) and phosphorus (%) in women, but not in men. The present results demonstrate that vitamin D is an important metabolic factor in skeletal muscle, and contributes to the optimal management of skeletal muscle and the prevention of sarcopenia. J. Med. Invest. 67 : 151-157, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114812 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.151 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378599 ● Search Scopus @ Elsevier (PMID): 32378599 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.151 (Tokushima University Institutional Repository: 114812, DOI: 10.2152/jmi.67.151, PubMed: 32378599)
7.	Mari Tajiri, Otoki Nakahashi, Tomohiro Kagawa, Masashi Masuda, Hirokazu Ohminami, Masayuki Iwano, Eiji Takeda, Yutaka Taketani and Hironori Yamamoto : Association of increased renal Cyp24a1 gene expression with low plasma 1,25-dihydroxyvitamin D levels in rats with streptozotocin-induced diabetes., Journal of Clinical Biochemistry and Nutrition, Vol.66, No.1, 49-56, 2019. (Summary) Decreases in plasma vitamin D concentrations have been reported in diabetes, although the mechanism involved in this decrease is unclear. Here, we investigated the association between Cyp24a1, a vitamin D catabolic enzyme, and abnormalities in vitamin D metabolism in streptozotocin-induced diabetes rats, an animal model of type 1 diabetes. Plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels were significantly lower in streptozotocin-induced diabetes rats and renal Cyp24a1 mRNA expression levels were increased. Western blotting analysis of streptozotocin-induced diabetes rats kidney tissues with anti-CYP24A1 antibody showed a strong signal around 40 kDa, which differs from the predicted 50-55 kDa molecular weight for full-length Cyp24a1 and could represent the Cyp24a1-splicing variant that lacks exons 1 and 2. We observed high levels of renal Cyp24a1-splicing variant mRNA expression in streptozotocin-induced diabetes rats. We also confirmed transcriptional up-regulation of endogenous Cyp24a1 mRNA expression through glucocorticoid receptors by glucocorticoid in opossum kidney proximal cells. Taken together, our results indicated that high Cyp24a1 expression levels may play a role in the decrease of plasma 1,25(OH)2D levels in streptozotocin-induced diabetes rats. High plasma corticosterone levels in diabetes may affect transcriptional regulation to promote increases in Cyp24a1 expression. (Tokushima University Institutional Repository) ● Metadata: 114242 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.19-79 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32001956 ● Search Scopus @ Elsevier (PMID): 32001956 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.19-79 (Tokushima University Institutional Repository: 114242, DOI: 10.3164/jcbn.19-79, PubMed: 32001956)
8.	Tomohiro Kagawa, Mina Kozai, Masashi Masuda, Nagakatsu Harada, Otoki Nakahashi, Mari Tajiri, Ryouhei Yoshikawa, Mari Nakao, Yuichiro Takei, Masayuki Iwano, Eiji Takeda, Yutaka Taketani and Hironori Yamamoto : 24-hydroxylase gene expression in renal proximal tubular cells., Biochemical and Biophysical Research Communications, Vol.500, No.2, 275-282, 2018. (Summary) ) showed dose-dependent reductions in renal Srebp1c and Cyp24a1 mRNA levels. Taken together, our results suggest that SREBP1 trans-activates CYP24A1 expression through SREBP binding elements present in the promoter. (Tokushima University Institutional Repository) ● Metadata: 112883 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2018.04.058 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29653103 ● Search Scopus @ Elsevier (PMID): 29653103 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.04.058 (Tokushima University Institutional Repository: 112883, DOI: 10.1016/j.bbrc.2018.04.058, PubMed: 29653103)
9.	Teruhiro Morishita, Michiko Sato, Hiroko Kume, Masae Sakuma, Hidekazu Arai, Takahumi Katayama, Shinsuke Katoh, Koichi Sairyo and Eiji Takeda : Skeletal muscle mass of old Japanese women suffering from walking difficulty in nursing home., The Journal of Medical Investigation : JMI, Vol.65, No.1.2, 122-130, 2018. (Summary) By using 24 hour urinary creatinine levels, skeletal muscle mass (kg), its rate (%) of body weight and creatinine height index (%) were determined in old Japanese women suffering from walking difficulty in nursing home and compare with those of young university students. Those of old subjects showed approximately 30-50%, 36-44% and 44-46% of young subjects, respectively. It is suggested that these values are important and useful biomarkers for the planning and the achievement of rehabilitation program for the maintaining and restoring skeletal muscle mass and for the careful support by registered care workers to aged persons. J. Med. Invest. 65:122-125, February, 2018. (Tokushima University Institutional Repository) ● Metadata: 111443 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.122 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593181 ● Search Scopus @ Elsevier (PMID): 29593181 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.122 (Tokushima University Institutional Repository: 111443, DOI: 10.2152/jmi.65.122, PubMed: 29593181)
10.	Ryouhei Yoshikawa, Hironori Yamamoto, Otoki Nakahashi, Tomohiro Kagawa, Mari Tajiri, Mari Nakao, Shiori Fukuda, Hidekazu Arai, Masashi Masuda, Masayuki Iwano, Eiji Takeda and Yutaka Taketani : The age-related changes of dietary phosphate responsiveness in plasma 1,25-dihydroxyvitamin D levels and renal Cyp27b1 and Cyp24a1 gene expression is associated with renal -Klotho gene expression in mice., Journal of Clinical Biochemistry and Nutrition, Vol.62, No.1, 68-74, 2017. (Summary) mRNA expression showed a significant negative correlation with plasma 1,25-dihydroxyvitamin D levels in the high phosphate group. Our results suggest that age-related alterations in renal -Klotho expression could affect the responsiveness of dietary phosphate to vitamin D metabolism. (Tokushima University Institutional Repository) ● Metadata: 111009 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.17-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29371756 ● Search Scopus @ Elsevier (PMID): 29371756 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.17-20 (Tokushima University Institutional Repository: 111009, DOI: 10.3164/jcbn.17-20, PubMed: 29371756)
11.	Kohei Sugihara, Masashi Masuda, Mari Nakao, Maerjianghan Abuduli, Yukiko Imi, Naoko Oda, Toshiya Okahisa, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : Dietary phosphate exacerbates intestinal inflammation in experimental colitis., Journal of Clinical Biochemistry and Nutrition, Vol.61, No.2, 91-99, 2017. (Summary) study, the effects of phosphate on proinflammatory cytokine induction and reactive oxygen species production in RAW264.7 macrophage were examined. Dietary phosphate exacerbated intestinal inflammation in experimental colitis in a dose-dependent manner, as assessed by the clinical disease activity score, colon length, and histology. Furthermore, the high phosphate diet increased myeloperoxidase activity and proinflammatory cytokine mRNA expression through the activation of nuclear factor B in the inflamed colon. In addition, high phosphate loading in RAW264.7 cells directly enhanced reactive oxygen species production and proinflammatory cytokine gene expression. Our results demonstrated that the high phosphate diet exacerbated intestinal inflammation in experimental colitis. These findings have important therapeutic implications for inflammatory bowel disease patients. (Tokushima University Institutional Repository) ● Metadata: 110124 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.16-117 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28955125 ● Search Scopus @ Elsevier (PMID): 28955125 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.16-117 (Tokushima University Institutional Repository: 110124, DOI: 10.3164/jcbn.16-117, PubMed: 28955125)
12.	Chisaki Adachi, Hisami Okumura, Takafumi Katayama, Yutaka Taketani and Eiji Takeda : Single vegetable meal content equivalence and alternative to fat for satiety: a randomised trial in Japanese women, Asia Pacific Journal of Clinical Nutrition, Vol.25, No.3, 478-486, 2016. (Summary) Although high energy density foods are highly palatable, their overconsumption leads to obesity because of high fat content. Low energy density foods are more effective for preventing individuals from becoming overweight. We investigated how different amounts of a single vegetable affect the sensory properties of meals with different energy densities. In a randomized crossover design, 40 young Japanese women consumed control and high-fat (HF) lunches. Control meals contained the same amount of rice and hamburger and 80 g (C80), 120 g (C120), 160 g (C160), 200 g (C200), 240 g (C240), or 280 g (C280) of broccoli. HF meals were control meals to which 38.1 g of oil was added (HF80, HF120, HF160, HF200, HF240, and HF280). Sensory properties before intake and 0.5, 1, 2, 3, 4, and 5 h after meals were assessed using a visual analog scale. Fullness was significantly lower with C80 than with C200 and C280 at 0.5 h and all time points, respectively, after consumption. In contrast, satisfaction with all HF meals was similar at all time points. Fullness and satisfaction were higher with almost all HF meals than with control meals; however, fullness and satisfaction were similar between HF200 and all control meals 1-4 h after consumption. Fat increases satiety when a single vegetable is included in the meal; however, at least of 200 g of vegetable in a 500- kcal meal with low fat content provides fullness and satisfaction similar to those provided by an HF meal. (Keyword) Adult / Cross-Over Studies / Diet, High-Fat / Dietary Fats / Energy Intake / Female / Humans / Meals / Satiation / Vegetables / Young Adult (Tokushima University Institutional Repository) ● Metadata: 109710 (Link to Publication Site) ● Publication site (DOI): 10.6133/apjcn.092015.25 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27440681 ● Summary page in Scopus @ Elsevier: 2-s2.0-84989767515 (Tokushima University Institutional Repository: 109710, DOI: 10.6133/apjcn.092015.25, PubMed: 27440681, Elsevier: Scopus)
13.	Maerjianghan Abuduli, Hirokazu Ohminami, Tamaki Otani, Hitoshi Kubo, Haruka Ueda, Yoshichika Kawai, Masashi Masuda, Hisami Okumura, Hiroshi Sakaue, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : Effects of dietary phosphate on glucose and lipid metabolism., American Journal of Physiology, Endocrinology and Metabolism, Vol.310, No.7, E526-E538, 2016. (Summary) Recent epidemiological and animal studies have suggested that excess intake of phosphate (Pi) is a risk factor for the progression of chronic kidney disease and its cardiovascular complications. However, little is known about the impact of dietary high Pi intake on the development of metabolic disorders such as obesity and type II diabetes. In this study, we investigated the effects of dietary Pi on glucose and lipid metabolism in healthy rats. Male, 8-wk-old Sprague-Dawley rats were divided into 3 groups and given experimental diets containing varying amounts of Pi, i.e. 0.2% (low Pi, LP), 0.6% (control Pi, CP), and 1.2% (high Pi, HP). After 4 weeks, HP group showed lower visceral fat accumulation compared with other groups, accompanied by a low respiratory exchange ratio (VCO2/VO2) without alteration of locomotive activity. HP group had lower levels of plasma insulin and non-esterified fatty acids. In addition, HP group also showed suppressed expression of hepatic lipogenic genes including sterol regulatory element binding protein-1c, fatty acid synthase, and acetyl-CoA carboxylase, whereas there was no difference in hepatic fat oxidation among the groups. On the other hand, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator alpha (PGC1) expression were significantly increased in the brown adipose tissue (BAT) of HP group. Our data demonstrated that a high Pi diet can negatively regulate lipid synthesis in the liver, and increased mRNA expression related to lipid oxidation and UCP1 in BAT, thereby preventing visceral fat accumulation. Thus, dietary Pi is a novel metabolic regulator. (Tokushima University Institutional Repository) ● Metadata: 109976 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00234.2015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26786774 ● Search Scopus @ Elsevier (PMID): 26786774 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00234.2015 (Tokushima University Institutional Repository: 109976, DOI: 10.1152/ajpendo.00234.2015, PubMed: 26786774)
14.	Mari Nakao, Hironori Yamamoto, Otoki Nakahashi, Shoko Ikeda, Kotaro Abe, Masashi Masuda, Mariko Ishiguro, Masayuki Iwano, Eiji Takeda and Yutaka Taketani : Dietary phosphate supplementation delays the onset of iron deficiency anemia and affects iron status in rats., Nutrition Research, Vol.35, No.11, 1016-1024, 2015. (Summary) Inorganic phosphate (Pi) plays critical roles in bone metabolism and is an essential component of 2,3-diphosphoglycerate (2,3-DPG). It has been reported that animals fed a low-iron diet modulate Pi metabolism, whereas the effect of dietary Pi on iron metabolism, particularly in iron deficiency anemia (IDA), is not fully understood. In this study, we hypothesized the presence of a link between Pi and iron metabolism and tested the hypothesis by investigating the effects of dietary Pi on iron status and IDA. Wistar rats aged 4 weeks were randomly assigned to 1 of 4 experimental dietary groups: normal iron content (Con Fe)+0.5% Pi, low-iron (Low Fe)+0.5% Pi, Con Fe+1.5% Pi, and Low Fe+1.5% Pi. Rats fed the 1.5% Pi diet for 14 days, but not for 28 days, maintained their anemia state and plasma erythropoietin concentrations within the reference range, even under conditions of low iron. In addition, plasma concentrations of 2,3-DPG were significantly increased by the 1.5% Pi diets and were positively correlated with plasma Pi concentration (r=0.779; P<.001). Dietary Pi regulated the messenger RNA expression of iron-regulated genes, including divalent metal transporter 1, duodenal cytochrome B, and hepcidin. Furthermore, iron concentration in liver tissues was increased by the 1.5% Pi in Con Fe diet. These results suggest that dietary Pi supplementation delays the onset of IDA and increases plasma 2,3-DPG concentration, followed by modulation of the expression of iron-regulated genes. (Tokushima University Institutional Repository) ● Metadata: 109711 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nutres.2015.09.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26475181 ● Search Scopus @ Elsevier (PMID): 26475181 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nutres.2015.09.001 (Tokushima University Institutional Repository: 109711, DOI: 10.1016/j.nutres.2015.09.001, PubMed: 26475181)
15.	Eiji Takeda, Hisami Okumura, Yutaka Taketani, Nobuya Inagaki, Masaya Hosokawa, Kenichiro Shide, Hiroshi Maegawa, Keiko Kondo, Eiji Kawasaki, Shoko Shinozaki, Yuichi Fujinaka, Tsukasa Matsubara, Takafumi Katayama, Hajime Sasaki, Akihiro Kawashima and Hiromitsu Aonuma : Effect of nutritional counseling and long term isomaltulose based liquid formula (MHN-01) intake on metabolic syndrome., Journal of Clinical Biochemistry and Nutrition, Vol.57, No.2, 140-144, 2015. (Summary) The isomaltulose based liquid formula (MHN-01), suppresses postprandial plasma glucose and insulin levels in healthy persons and patients with impaired glucose tolerance (IGT) or type 2 diabetes. MHN-01 intake as a part of breakfast also suppresses glucose and insulin levels after lunch, suggesting second meal effect. The objective of this study was to investigate the effects of nutritional counseling and long-term (24 weeks) MHN-01 ingestion on biomarkers of metabolic syndrome. Forty-one subjects with criteria of metabolic syndrome participated in this study composed with the control period (0-12 week) followed by nutritional counseling and the experimental period (12-36 week) followed by 200 kcal (837 kJ) of MHN-01 or dextrin-based standard balanced liquid formula (SBF) loading as a part of breakfast. In 16 of 41 subjects became to out of criteria for liquid formula loading study during control period (unqualified group). In the unqualified group, several biomarkers were improved. In experimental period, serum HbA1c levels significantly increased in SBF group (n = 12) but did not change in MHN-01 group (n = 10). Thus, intake of 837 kJ MHN-01 as a part of breakfast may be effective for suppression of deteriorating glucose metabolism in metabolic syndrome. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.14-132 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26388672 ● Search Scopus @ Elsevier (PMID): 26388672 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.14-132 (DOI: 10.3164/jcbn.14-132, PubMed: 26388672)
16.	Yuka Kawakami, Hisami Okumura, Yuko Naniwa-Kuroki, Masae Sakuma, Yutaka Taketani and Eiji Takeda : Flaxseed oil intake reduces serum small dense low-density lipoprotein concentrations in Japanese men: a randomized, double blind, crossover study., Nutrition Journal, Vol.14, 39, 2015. (Summary) This study indicates that the FO, which is a rich source of ALA, leads to lower sd-LDL cholesterol concentrations. (Link to Publication Site) ● Publication site (DOI): 10.1186/s12937-015-0023-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25896182 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928333962 (DOI: 10.1186/s12937-015-0023-2, PubMed: 25896182, Elsevier: Scopus)
17.	Kohei Sugihara, Hisami Okumura, Arisa Teramoto, Eri Urano, Takafumi Katayama, Yuji Morine, Satoru Imura, Tohru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Recovery of nutritional metabolism after liver transplantation, Nutrition, Vol.31, No.1, 105-110, 2015. (Summary) Perioperative nutritional assessment is critically important to reflect nutritional management because liver transplantation (LTx) often is undertaken in patients with poor nutritional status. The aim of this study was to evaluate nutritional status, including the non-protein respiratory quotient (npRQ), resting energy expenditure (REE), nitrogen balance, and blood biochemical parameters in patients before and after LTx. Fourteen patients undergoing LTx and 10 healthy controls were enrolled in this study. The npRQ and REE were measured using indirect calorimetry before LTx and at 2, 3, and 4 wk after the procedure. Blood biochemistry and nitrogen balance calculated by 24-h urine collection were performed concurrently with indirect calorimetric measurement; the results were compared between the two groups. Before LTx, npRQ was significantly lower and serum non-esterified fatty acid levels were significantly higher in the patients than in the controls. Furthermore, a negative nitrogen balance was observed in the patients. These, however, improved significantly at 4 wk after LTx. REE did not significantly increase compared with the preoperative values in recipients. Blood biochemistry showed gradually increasing levels of serum cholinesterase and albumin. These failed to reach to normal levels by 4 wk post-transplant. The findings revealed that improvement of nutritional metabolism after LTx may require 4 wk. Additional nutritional strategies, therefore, may be needed to minimize catabolic state during the early post-transplant period. Adequate, individualized nutritional guidance before and after LTx should be performed in these patients. (Keyword) Body Mass Index / Body Weight / Calorimetry, Indirect / Case-Control Studies / Cholinesterases / energy metabolism / Fatty Acids, Nonesterified / Female / Humans / Liver Transplantation / Male / Middle Aged / Nitrogen / Nutrition Assessment / Nutritional Status / Perioperative Care / Serum Albumin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nut.2014.05.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25441593 ● Summary page in Scopus @ Elsevier: 2-s2.0-84922214411 (DOI: 10.1016/j.nut.2014.05.016, PubMed: 25441593, Elsevier: Scopus)
18.	Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto : Niacin and Chronic Kidney Disease., Journal of Nutritional Science and Vitaminology, Vol.61 Suppl, S173-5, 2015. (Summary) Chronic kidney disease (CKD) is an increasing problem worldwide. The number of end-stage renal disease patients requiring treatment by dialysis is estimated to be increasing by 10,000 patients per year in Japan. Furthermore, an estimated 13 million people are living with CKD in Japan. Various complications are associated with CKD, including cardiovascular disease (CVD). More than one-third of CKD patients die from CVD. Thus, prevention of CVD is a primary concern for the treatment of CKD patients. CKD-mineral and bone disorder (CKD-MBD) is a serious complication that typically leads to CVD. Hyperphosphatemia is thought to be a central-risk factor for CKD-MBD. Therefore, managing hyperphosphatemia is crucial to prevent CKD-MBD and CVD. It is difficult to achieve the target serum phosphate level through dietary modifications alone in patients with hyperphosphatemia, because most foods contain phosphate. Thus, phosphate binders such as calcium carbonate are commonly prescribed to CKD patients with hyperphosphatemia, but these have undesirable side effects. Inhibition of intestinal phosphate transport activity has also been investigated as an alternative approach for controlling serum phosphate levels in CKD patients. Nicotinamide, which is the amide of niacin, can inhibit intestinal phosphate transport. Niacin and related compounds have also been developed as drugs for hyperlipidemia conditions, especially hypertriglyceridemia with low high-density lipoprotein. This type of dyslipidemia is frequently observed in CKD patients and is a modifiable risk factor for CVD. Thus, niacin and related compounds may have utility for the treatment of both hyperphosphatemia and dyslipidemia in CKD patients to prevent CVD. (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.61.S173 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26598845 ● Summary page in Scopus @ Elsevier: 2-s2.0-84950314636 (DOI: 10.3177/jnsv.61.S173, PubMed: 26598845, Elsevier: Scopus)
19.	Eriko Watari, Yutaka Taketani, Tomoyo Kitamura, Terumi Tanaka, Hirokazu Ohminami, Maerjianghan Abuduli, Nagakatsu Harada, Hisami Yamanaka-Okumura, Hironori Yamamoto and Eiji Takeda : Fluctuating plasma phosphorus level by changes in dietary phosphorus intake induces endothelial dysfunction., Journal of Clinical Biochemistry and Nutrition, Vol.56, No.1, 35-42, 2014. (Summary) High serum phosphorus (P) impairs endothelial function by increasing oxidative stress and decreasing nitric oxide production. Serum P levels fluctuate due to circadian rhythms or dietary P intake in healthy people and due to dialysis in end-stage chronic kidney disease patients. Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk. Rats were fed a diet containing 0.6% P for 16 days (control group), or a diet alternating between 0.02% P and 1.2% P (LH group) or between 1.2% P and 0.02% P (HL group) every 2 days; the total amount of P intake among the groups during the feeding period was similar. In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group. These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response. Taken together, these results suggest that habitual fluctuation of dietary P intake might be a cause of cardiovascular disease through endothelial dysfunction, especially in chronic kidney disease patients. (Tokushima University Institutional Repository) ● Metadata: 106333 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.14-96 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25678749 ● Search Scopus @ Elsevier (PMID): 25678749 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.14-96 (Tokushima University Institutional Repository: 106333, DOI: 10.3164/jcbn.14-96, PubMed: 25678749)
20.	B Zhou, Hisami Okumura, C Adachi, Y Kawakami, Takafumi Katayama and Eiji Takeda : High-fat diet-related stimulation of sweetness desire is greater in women than in men despite high vegetable intake, Public Health Nutrition, Vol.18, No.7, 1272-1281, 2014. (Summary) To examine the effects of lunches with different dietary energy densities on food preferences between genders. Randomized crossover study. Participants were administered the following packed test meals once weekly on a specified day during six sessions: control (150 g of rice with a sautéed beef entrée containing 40 g of raw beef and 240 g of vegetables), high-meat/low-rice, low-vegetable, medium-fat/low-vegetable, high-fat and high-fat/low-vegetable meals. Subjective levels of sensory properties were assessed over time using visual analogue scales. University of Tokushima Graduate School, Tokushima, Japan. Sixty-five men and sixty-five women matched by age and BMI. Men showed significantly stronger desires for salty and fatty foods after meals (P<0·05). Women showed a significantly stronger desire for sweetness from 2 h after the low-vegetable meal, and increasing fat content under high-vegetable conditions caused a significant stimulated sweetness desire in women more than in men (P<0·05). Moreover, after a high-meat/low-rice meal with 100 g of rice, sweetness desire was stronger in women (P=0·024), whereas no significant differences in sweetness desire were shown between genders after another low-energy-density control meal with 150 g of rice. Men had significantly stronger desires for salty and fatty foods, whereas women preferred sweet food after meals. The sweetness desire in women was stimulated by increasing fat content, even with a high vegetable intake. Low rice intake in a low-energy-density diet also caused a relative stimulation of sweetness desire in women. (Keyword) Appetite Regulation / Cross-Over Studies / Diet, High-Fat / Diet, Reducing / Dietary Fats / Energy Intake / Female / Food Preferences / Humans / Japan / Lunch / Male / Postprandial Period / Sex Characteristics / Sodium Chloride, Dietary / Sweetening Agents / Vegetables (Link to Publication Site) ● Publication site (DOI): 10.1017/S1368980014001426 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25079560 ● Search Scopus @ Elsevier (PMID): 25079560 ● Search Scopus @ Elsevier (DOI): 10.1017/S1368980014001426 (DOI: 10.1017/S1368980014001426, PubMed: 25079560)
21.	Hirokazu Ohminami, Kikuko Amou, Yutaka Taketani, Kazusa Sato, Makiko Fukaya, Takashi Uebanso, Hidekazu Arai, Megumi Koganei, Hajime Sasaki, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Dietary combination of sucrose and linoleic acid causes skeletal muscle metabolic abnormalities in Zucker fatty rats through specific modification of fatty acid composition., Journal of Clinical Biochemistry and Nutrition, Vol.55, No.1, 15-25, 2014. (Summary) A dietary combination of sucrose and linoleic acid strongly contributes to the development of metabolic disorders in Zucker fatty rats. However, the underlying mechanisms of the metabolic disorders are poorly understood. We hypothesized that the metabolic disorders were triggered at a stage earlier than the 8 weeks we had previously reported. In this study, we investigated early molecular events induced by the sucrose and linoleic acid diet in Zucker fatty rats by comparison with other combinations of carbohydrate (sucrose or palatinose) and fat (linoleic acid or oleic acid). Skeletal muscle arachidonic acid levels were significantly increased in the sucrose and linoleic acid group compared to the other dietary groups at 4 weeks, while there were no obvious differences in the metabolic phenotype between the groups. Expression of genes related to arachidonic acid synthesis was induced in skeletal muscle but not in liver and adipose tissue in sucrose and linoleic acid group rats. In addition, the sucrose and linoleic acid group exhibited a rapid induction in endoplasmic reticulum stress and abnormal lipid metabolism in skeletal muscle. We concluded that the dietary combination of sucrose and linoleic acid primarily induces metabolic disorders in skeletal muscle through increases in arachidonic acid and endoplasmic reticulum stress, in advance of systemic metabolic disorders. (Tokushima University Institutional Repository) ● Metadata: 106169 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.14-11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25147427 ● Search Scopus @ Elsevier (PMID): 25147427 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.14-11 (Tokushima University Institutional Repository: 106169, DOI: 10.3164/jcbn.14-11, PubMed: 25147427)
22.	Yuuka Morimoto, Masae Sakuma, Hiroyuki Ohta, Akitsu Suzuki, Asami Matsushita, Minako Umeda, Makoto Ishikawa, Yutaka Taketani, Eiji Takeda and Hidekazu Arai : Estimate of dietary phosphorus intake using 24-h urine collection., Journal of Clinical Biochemistry and Nutrition, Vol.55, No.1, 62-66, 2014. (Summary) Increases in serum phosphorus levels and dietary phosphorus intake induces vascular calcification, arterial sclerosis and cardiovascular diseases. Limiting phosphorus intake is advisable, however, no assessment methods are capable of estimating dietary phosphorus intake. We hypothesized that urinary phosphorus excretion can be translated into estimation of dietary phosphorus intake, and we evaluated whether a 24-h urine collection method could estimate dietary phosphorus intake. Thirty two healthy subjects were recruited for this study. Subjects collected urine samples over 24 h and weighed dietary records. We calculated dietary protein intake and phosphorus intake from dietary records and urine collection, and investigated associations between the two methods in estimating protein and phosphorus intake. Significant positive correlations were observed between dietary records and UC for protein and phosphorus intake. The average intakes determined from dietary records were significantly higher than from urine collection for both protein and phosphorus. There was a significant positive correlation between both the phosphorus and protein difference in dietary records and urine collection. The phosphorus-protein ratio in urine collection was significantly higher than in dietary records. Our data indicated that the 24-h urine collection method can estimate the amount of dietary phosphorus intake, and the results were superior to estimation by weighed dietary record. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.14-15 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25120281 ● Search Scopus @ Elsevier (PMID): 25120281 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.14-15 (DOI: 10.3164/jcbn.14-15, PubMed: 25120281)
23.	KKohei Sugihara, Hisami Okumura, Arisa Teramoto, Eri Urano, Takafumi Katayama, Hiroki Mori, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Recovery pattern of non-protein respiratory quotient and non-esterified fatty acid after liver resection, Nutrition, Vol.30, No.4, 443-448, 2014. (Summary) Perioperative nutritional care is important to maintain preoperative and postoperative nutritional status. However, few reports have investigated energy metabolism after hepatectomy. The aim of this study was to determine differences in energy metabolism, blood biochemistry, and nutritional status before and after liver resection in patients with hepatocellular carcinoma (HCC) and healthy living donors for liver transplantation. Eighteen hospitalized patients with HCC group and 13 living donors for liver transplantation (donor group) were enrolled in this study. The donor group was divided into two groups on the basis of age; Y-donor group (age < 40 y, n = 7), and O-donor group (age ≥ 40 y, n = 6). Energy metabolism was measured by indirect calorimetry at preoperative day and postoperative day (POD) 7 and 14, and blood biochemistry was also examined. Recovery of non-protein respiratory quotient (npRQ) and blood biochemical data such as total bilirubin, aspartate aminotransferase and alanine aminotransferase levels were observed in Y-donor group on POD 14. However, although biochemical data improved in the HCC and O-donor group, npRQ remained unchanged on POD 14. Improvement of npRQ took longer than blood biochemical data in patients with HCC and older donors. Because the recovery of npRQ is associated with donor age, careful nutritional management may be required for a longer time depending on the pathophysiological condition of each patient after hepatectomy. (Keyword) Adult / Age Factors / Aged / Alanine Transaminase / Aspartate Aminotransferases / Bilirubin / Calorimetry, Indirect / Carcinoma, Hepatocellular / energy metabolism / Fatty Acids, Nonesterified / Female / Hepatectomy / Hospitalization / Humans / Liver / Liver Neoplasms / Liver Transplantation / Living Donors / Male / Middle Aged / Nutritional Status / Postoperative Care / Postoperative Period / Young Adult (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nut.2013.09.012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24332605 ● Summary page in Scopus @ Elsevier: 2-s2.0-84895475137 (DOI: 10.1016/j.nut.2013.09.012, PubMed: 24332605, Elsevier: Scopus)
24.	Otoki Nakahashi, Hironori Yamamoto, Sarasa Tanaka, Mina Kozai, Yuichiro Takei, Masashi Masuda, Ichiro Kaneko, Yutaka Taketani, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda : Short-term dietary phosphate restriction up-regulates ileal fibroblast growth factor 15 gene expression in mice., Journal of Clinical Biochemistry and Nutrition, Vol.54, No.2, 102-108, 2014. (Summary) Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy. It has been reported that dietary Pi regulates circulating FGF23. In this study, the short-term effects of dietary Pi restriction on the expression of FGF19 subfamily members in mice were analyzed. An initial analysis confirmed plasma FGF23 levels positively correlated with the amount of dietary Pi. On the other hand, ileal Fgf15 gene expression, but not hepatic Fgf21 gene expression, was up-regulated by dietary Pi restriction. In addition, we observed the increase of plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels by dietary Pi restriction, and the up-regulation of ileal Fgf15 mRNA expression by 1,25(OH)2D3 and vitamin D receptor (VDR). Importantly, dietary Pi restriction-induced Fgf15 gene expression was prevented in VDR-knockout mice. Furthermore, diurnal variations of plasma triglyceride concentrations and hepatic mRNA expression of the bile acid synthesis enzyme Cyp7a1 as one of Fgf15 negative target genes was influenced by dietary Pi restriction. These results suggest that dietary Pi restriction up-regulates ileal Fgf15 gene expression through 1,25(OH)2D3 and VDR, and may affect hepatic bile acid homeostasis. (Tokushima University Institutional Repository) ● Metadata: 106159 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.13-109 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24688219 ● Search Scopus @ Elsevier (PMID): 24688219 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.13-109 (Tokushima University Institutional Repository: 106159, DOI: 10.3164/jcbn.13-109, PubMed: 24688219)
25.	Shoko Ikeda, Hironori Yamamoto, Masashi Masuda, Yuichiro Takei, Otoki Nakahashi, Mina Kozai, Sarasa Tanaka, Mari Nakao, Yutaka Taketani, Hiroko Segawa, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda : Downregulation of renal type IIa sodium-dependent phosphate cotransporter during lipopolysaccharide-induced acute inflammation., American Journal of Physiology, Renal Physiology, Vol.306, No.7, F744-50, 2014. (Summary) The type IIa sodium-dependent phosphate cotransporter (Npt2a) plays a critical role in reabsorption of inorganic phosphate (Pi) by renal proximal tubular cells. Pi abnormalities during early stages of sepsis have been reported, but the mechanisms regulating Pi homeostasis during acute inflammation are poorly understood. We examined the regulation of Pi metabolism and renal Npt2a expression during lipopolysaccharide (LPS)-induced inflammation in mice. Dose-response and time-course studies with LPS showed significant increases of plasma Pi and intact parathyroid hormone (iPTH) levels and renal Pi excretion, while renal calcium excretion was significantly decreased. There was no difference in plasma 1,25-dihydroxyvitamin D levels, but the induction of plasma intact fibroblast growth factor 23 levels peaked 3 h after LPS treatment. Western blotting, immunostaining, and quantitative real-time PCR showed that LPS administration significantly decreased Npt2a protein expression in the brush border membrane (BBM) 3 h after injection, but there was no change in renal Npt2a mRNA levels. Moreover, tumor necrosis factor- injection also increased plasma iPTH and decreased renal BBM Npt2a expression. Importantly, we revealed that parathyroidectomized rats had impaired renal Pi excretion and BBM Npt2a expression in response to LPS. These results suggest that the downregulation of Npt2a expression in renal BBM through induction of plasma iPTH levels alter Pi homeostasis during LPS-induced acute inflammation. (Keyword) Acute Disease / Animals / Calcium / Disease Models, Animal / Down-Regulation / Fibroblast Growth Factors / Inflammation / Injections, Intraperitoneal / Kidney / Lipopolysaccharides / Male / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Microvilli / Parathyroid Hormone / Parathyroidectomy / Phosphates / RNA, Messenger / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Time Factors / Tumor Necrosis Factor-alpha / Vitamin D (Tokushima University Institutional Repository) ● Metadata: 106168 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00474.2013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24500689 ● Search Scopus @ Elsevier (PMID): 24500689 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00474.2013 (Tokushima University Institutional Repository: 106168, DOI: 10.1152/ajprenal.00474.2013, PubMed: 24500689)
26.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : Increasing dietary phosphorus intake from food additives: potential for negative impact on bone health., Advances in Nutrition, Vol.5, No.1, 92-97, 2014. (Summary) It is important to consider whether habitual high phosphorus intake adversely affects bone health, because phosphorus intake has been increasing, whereas calcium intake has been decreasing in dietary patterns. A higher total habitual dietary phosphorus intake has been associated with higher serum parathyroid hormone (PTH) and lower serum calcium concentrations in healthy individuals. Higher serum PTH concentrations have been shown in those who consume foods with phosphorus additives. These findings suggest that long-term dietary phosphorus loads and long-term hyperphosphatemia may have important negative effects on bone health. In contrast, PTH concentrations did not increase as a result of high dietary phosphorus intake when phosphorus was provided with adequate amounts of calcium. Intake of foods with a ratio of calcium to phosphorus close to that found in dairy products led to positive effects on bone health. Several randomized controlled trials have shown positive relations between dairy intake and bone mineral density. In our loading test with a low-calcium, high-phosphorus lunch provided to healthy young men, serum PTH concentrations showed peaks at 1 and 6 h, and serum fibroblast growth factor 23 (FGF23) concentrations increased significantly at 8 h after the meal. In contrast, the high-calcium, high-phosphorus meal suppressed the second PTH and FGF23 elevations until 8 h after the meal. This implies that adequate dietary calcium intake is needed to overcome the interfering effects of high phosphorus intake on PTH and FGF23 secretion. FGF23 acts on the parathyroid gland to decrease PTH mRNA and PTH secretion in rats with normal kidney function. However, increased serum FGF23 is an early alteration of mineral metabolism in chronic kidney disease, causing secondary hyperthyroidism, and implying resistance of the parathyroid gland to the action of FGF23 in chronic kidney disease. These findings suggest that long-term high-phosphorus diets may impair bone health mediated by FGF23 resistance both in chronic kidney disease patients and in the healthy population. (Link to Publication Site) ● Publication site (DOI): 10.3945/an.113.004002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24425727 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907167985 (DOI: 10.3945/an.113.004002, PubMed: 24425727, Elsevier: Scopus)
27.	B Zhou, Hisami Okumura, S Seki, H Tatano, C Adachi and Eiji Takeda : What influences appetite more: eating approaches or cooking methods?, The Journal of Medical Investigation : JMI, Vol.61, No.1.2, 118-125, 2014. (Summary) In general, vegetables are abundantly consumed in a calorie-restricted diet to achieve sufficient satiety through fresh food or various cooking methods. In this study, we examined the effects of different cooking methods on appetite and specific perceptions of the food after consumption; eating approaches were also analyzed by meal duration. A total of 153 individuals aged 20-59 years were assigned to 2 groups: raw vegetable or boiled vegetable meals, including packed meals that were served as test meals with the same energy and vegetable amount. Subjective levels of sensory properties and meal duration were assessed over time using visual analog scales, including questionnaires. Results showed that meal duration was significantly longer for raw vegetable meals than boiled vegetable meals, and there were significantly stronger correlations between meal duration and fullness. A higher degree of fullness was provided by a raw vegetable meal than a boiled vegetable meal, especially in men. However, an excess of raw vegetables led to overall insufficient satisfaction. Taken together, these findings suggest that cooking methods should be altered for different situations with an adequate amount of vegetables, and the meal duration should be recommended to be given as much attention as cooking methods. J. Med. Invest. 61: 118-125, February, 2014 (Keyword) appetite sensation / raw vegetable / boiled vegetable / meal duration / visual analog scales (Tokushima University Institutional Repository) ● Metadata: 109528 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.118 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705757 ● CiNii @ National Institute of Informatics (CRID): 1390282679221873152 ● Search Scopus @ Elsevier (PMID): 24705757 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.61.118 (Tokushima University Institutional Repository: 109528, DOI: 10.2152/jmi.61.118, PubMed: 24705757, CiNii: 1390282679221873152)
28.	A Teramoto, Hisami Okumura, E Urano, T Nakamura-Kutsuzawa, K Sugihara, Takafumi Katayama, Hidenori Miyake, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Comparison of measured and predicted energy expenditure in patients with liver cirrhosis, Asia Pacific Journal of Clinical Nutrition, Vol.23, No.2, 197-204, 2014. (Summary) Obesity is a risk factor for the onset of liver cancer in patients with cirrhosis. To prevent overfeeding and obesity, estimation of energy requirement is important, but energy expenditure in patients with liver cirrhosis has not been fully elucidated. This study aimed to investigate resting energy expenditure (REE) and energy intake in patients with cirrhosis and determine adequate energy intake criteria. In this cross-sectional study, indirect calorimetry measurement was conducted in 488 Japanese inpatients with cirrhosis. We compared REE measured by indirect calorimetry (M-REE) with basal energy expenditure (BEE) predicted by the Harris-Benedict equation (H-BEE) and Dietary Reference Intakes (DRI) for Japanese (D-BEE). Mean M-REE (1256 kcal) was significantly lower than H-BEE (1279 kcal); however, it was not significantly different from D-BEE (1254 kcal). Mean M-REE expressed in relation to body weight (BW; REE/kg BW) was 21.7 kcal/kg BW. H-BEE was significantly higher than M-REE in patients in the first and second quartiles of BMI, and D-BEE was significantly different from MREE in patients in the highest and lowest quartiles of BMI. Average energy intake was 30.5 kcal/kg BW, which was 1.4 times greater than REE/kg BW. Although DRI is a useful tool for the estimation of REE in patients in the second and third quartiles of BMI, M-REE is recommended to ensure the provision of adequate nutritional care to patients with cirrhosis, including those in the highest and lowest quartiles of BMI. (Keyword) Basal Metabolism / Body Mass Index / Calorimetry, Indirect / Cross-Sectional Studies / Energy Metabolism / Female / Humans / Japan / Liver Cirrhosis / Male / Middle Aged (Link to Publication Site) ● Publication site (DOI): 10.6133/apjcn.2014.23.2.12 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24901087 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905192746 (DOI: 10.6133/apjcn.2014.23.2.12, PubMed: 24901087, Elsevier: Scopus)
29.	Yutaka Taketani, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Role of nutrient transporters in lifestyle-related diseases, The Journal of Physical Fitness and Sports Medicine, Vol.2, No.4, 409-416, 2013. (Summary) Nutrient transporters play significant roles in physiological hormonal and cellular functions as well as in the maintenance of nutrient metabolism. Lifestyle-related disease can be defined as caused by a disturbance in nutrient metabolism as found in diabetes, dyslipidemia, arteriosclerosis, etc. Therefore, deterioration of nutrient transporters by a genetic mutation or abnormal regulation would cause various lifestyle-related diseases. For instance, dysregulation of muscular glucose transport causes hyperglycemia, and impairment of pancreatic glucose transport can be related to inadequate insulin secretion. These deleterious changes in glucose transport can be a cause of diabetes mellitus. Here, we introduce some examples that indicate the relationship between impairment of nutrient transporters and development of lifestyle-related diseases. (Keyword) transporter / nutrient homeostasis / polymorphism / lifestyle-related disease (Link to Publication Site) ● Publication site (DOI): 10.7600/jpfsm.2.409 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205415412992 ● Search Scopus @ Elsevier (DOI): 10.7600/jpfsm.2.409 (DOI: 10.7600/jpfsm.2.409, CiNii: 1390001205415412992)
30.	Wanjiku Violet Wanjihia, Hirokazu Ohminami, Yutaka Taketani, Kikuko Amou, Hisami Yamanaka-Okumura, Hironori Yamamoto and Eiji Takeda : Induction of the hepatic stearoyl-CoA desaturase 1 gene in offspring after isocaloric administration of high fat sucrose diet during gestation., Journal of Clinical Biochemistry and Nutrition, Vol.53, No.3, 150-157, 2013. (Summary) Adverse early nutrition leads to metabolic aberrations in adulthood. Molecular and cellular mechanisms responsible are emerging; specific nutritional causes remain unclarified. We investigated gestational dietary intake and its influences on metabolism in offspring. Three groups of pregnant Sprague-Dawley rats were fed either AIN93G standard diet as control, isocaloric high fat sucrose diet or calorie restriction diet (50% of control) until delivery. All dams were fed control diet ad libitum during lactation. Offsprings' metabolic parameters were assessed at three weeks. Visceral fat and plasma triglycerides of high fat sucrose diet offspring were significantly higher than those of control diet and calorie restriction diet offspring. Plasma leptin level was higher in high fat sucrose diet than control offspring. Conversely, plasma adiponectin was lower in high fat sucrose diet and calorie restriction diet offspring compared to controls. Significant inductions of hepatic mRNA expression of stearoyl-CoA desaturase1 and -5 desaturase genes, were observed in high fat sucrose diet and calorie restriction diet offspring. Gestational high sugar and fat intake even without over energy intake would be more detrimental to metabolisms of offspring compared to calorie restriction. (Tokushima University Institutional Repository) ● Metadata: 105925 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.13-48 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24249969 ● Search Scopus @ Elsevier (PMID): 24249969 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.13-48 (Tokushima University Institutional Repository: 105925, DOI: 10.3164/jcbn.13-48, PubMed: 24249969)
31.	Yuka Kawakami, Hisami Okumura, Masae Sakuma, Yuka Mori, Chisaki Adachi, Yukie Matsumoto, Tadatoshi Sato, Hironori Yamamoto, Yutaka Taketani, Takafumi Katayama and Eiji Takeda : Gene expression profiling in peripheral white blood cells in response to the intake of food with different glycemic index using a DNA microarray., Journal of Nutrigenetics and Nutrigenomics, Vol.6, No.3, 154-168, 2013. (Summary) Gene expression profiling in the WBC can reflect food-related metabolic changes, even in the postprandial state. (Keyword) Blood Glucose / Cross-Over Studies / Gene Expression Profiling / Glycemic Index / Humans / Insulin / Leukocytes / Male / Oligonucleotide Array Sequence Analysis / Transcriptome (Tokushima University Institutional Repository) ● Metadata: 109379 (Link to Publication Site) ● Publication site (DOI): 10.1159/000354247 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24008923 ● Search Scopus @ Elsevier (PMID): 24008923 ● Search Scopus @ Elsevier (DOI): 10.1159/000354247 (Tokushima University Institutional Repository: 109379, DOI: 10.1159/000354247, PubMed: 24008923)
32.	Sarasa Tanaka, Hironori Yamamoto, Otoki Nakahashi, Tomohiro Kagawa, Mariko Ishiguro, Masashi Masuda, Mina Kozai, Shoko Ikeda, Yutaka Taketani and Eiji Takeda : Dietary phosphate restriction induces hepatic lipid accumulation through dysregulation of cholesterol metabolism in mice., Nutrition Research, Vol.33, No.7, 586-593, 2013. (Summary) Excessive inorganic phosphate (Pi) intake and hyperphosphatemia have both been speculated to be risk factors for cardiovascular disease and hypercholesterolemia, and dysregulation of cholesterol metabolism can lead to atherosclerosis. However, the relationship between Pi and cholesterol metabolism has not been investigated in detail. Our recent study showed that triiodothyronine can induce both hyperphosphatemia and hypocholesterolemia in mice. We therefore hypothesized a possible linkage between Pi and cholesterol metabolism. In this study, we investigated the effects of dietary Pi intake on cholesterol metabolism in mice. Mice were divided into 4 groups, which were fed diets containing 1.2% or 0.1% Pi and with or without 2% cholesterol (Pi-sufficient, Pi-restricted, Pi-sufficient + Chol, and Pi-restricted + Chol), for 12 days. Inorganic phosphate-restricted mice exhibited significantly higher liver weights than did Pi-sufficient mice. Interestingly, dietary Pi restriction significantly increased high-cholesterol diet-induced hepatic lipid accumulation. Real-time polymerase chain reaction analysis revealed that dietary Pi restriction decreased expression of hepatic genes involved in cholesterol metabolism and fatty acid biosynthesis. In addition, hepatic messenger RNA levels of several transcription factors including peroxisome proliferator-activated receptors and liver X receptor were markedly decreased by Pi restriction. Furthermore, plasma lipid and lipoprotein profile analysis showed that dietary Pi restriction reduced susceptibility to high-cholesterol diet-induced hyperlipidemia. Importantly, we found that there was a significant negative correlation between plasma levels of Pi and total cholesterol. These results suggest that dietary Pi plays an important role in the development of fatty liver disease and hyperlipidemia induced by a high-cholesterol diet through regulation of lipid metabolism-related gene expression in the liver. (Keyword) Animals / Cholesterol / Cholesterol, Dietary / Diet / Fatty Acids / Fatty Liver / Gene Expression / Gene Expression Regulation / Hyperlipidemias / Lipid Metabolism / Lipids / Lipoproteins / Liver / Male / Mice / Mice, Inbred C57BL / Organ Size / Orphan Nuclear Receptors / Peroxisome Proliferator-Activated Receptors / Phosphates / RNA, Messenger / Transcription Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nutres.2013.05.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23827134 ● Search Scopus @ Elsevier (PMID): 23827134 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nutres.2013.05.004 (DOI: 10.1016/j.nutres.2013.05.004, PubMed: 23827134)
33.	Mina Kozai, Hironori Yamamoto, Mariko Ishiguro, Nagakatsu Harada, Masashi Masuda, Tomohiro Kagawa, Yuichiro Takei, Ayako Otani, Otoki Nakahashi, Shoko Ikeda, Yutaka Taketani, Ken-Ichi Takeyama, Shigeaki Kato and Eiji Takeda : Thyroid hormones decrease plasma 1,25-dihydroxyvitamin D levels through transcriptional repression of the renal 25-hydroxyvitamin D3 1-hydroxylase gene (CYP27B1)., Endocrinology, Vol.154, No.2, 609-622, 2013. (Summary) The primary determinant of circulating 1,25-dihydroxyvitamin D (1,25[OH](2)D) levels is the activity of 25-hydroxyvitamin D-1-hydroxylase (cytochrome P450 27B1 [CYP27B1]) in the kidney. Hyperthyroid patients have been reported to have low levels of plasma 1,25(OH)(2)D. However, the detailed mechanism of thyroid hormone action on vitamin D metabolism is still poorly understood. The present study determined whether renal CYP27B1 gene expression was negatively regulated by thyroid hormones. T(3)-induced hyperthyroid mice showed marked decreases in plasma 1,25(OH)(2)D levels and in renal expression of CYP27B1 mRNA but no changes in plasma concentrations of calcium, PTH, or fibroblast growth factor-23. In addition, we observed that T(3) administration significantly decreased plasma 1,25(OH)(2)D and renal CYP27B1 mRNA levels that were increased by low-calcium or low-phosphorus diets and induced hypocalcemia in mice fed a low-calcium diet. Promoter analysis revealed that T(3) decreases the basal transcriptional activity of the CYP27B1 gene through thyroid hormone receptors (TR and TR1) and the retinoid X receptor (RXR) in renal proximal tubular cells. Interestingly, we identified an everted repeat negative thyroid hormone response element (1-nTRE) overlapping the sterol regulatory element (1-SRE) and the TATA-box -50 to -20 base pairs from the human CYP27B1 gene transcription start site. Finally, we established that CYP27B1 gene transcription is positively regulated by SRE-binding proteins and that a T(3)-bound TR1/RXR heterodimer inhibits SRE-binding protein-1c-induced transcriptional activity through the 1-nTRE. These results suggest that transcriptional repression of the CYP27B1 gene by T(3)-bound TRs/RXR, acting through the 1-nTRE, results in decreased renal CYP27B1 expression and plasma 1,25(OH)(2)D levels. (Keyword) 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / Animals / Calcitriol / Enzyme Repression / Humans / Kidney / Kidney Tubules, Proximal / Mice / RNA, Messenger / Response Elements / Thyroid Hormones / Transcription, Genetic / Triiodothyronine (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2012-1647 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23307792 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872702811 (DOI: 10.1210/en.2012-1647, PubMed: 23307792, Elsevier: Scopus)
34.	Sarasa Tanaka, Hironori Yamamoto, Otoki Nakahashi, Mariko Ishiguro, Yuichiro Takei, Masashi Masuda, Mina Kozai, Shoko Ikeda, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Hypercholesterolemia and effects of high cholesterol diet in type IIa sodium-dependent phosphate co-transporter (Npt2a) deficient mice., The Journal of Medical Investigation : JMI, Vol.60, No.3-4, 191-196, 2013. (Summary) The type IIa sodium-dependent phosphate co-transporter (Npt2a) is important to maintain renal inorganic phosphate (Pi) homeostasis and the plasma Pi levels. It has reported that disorder of Pi metabolism in kidney can be risk factors for cardiovascular disease as well as hypercholesterolemia. However, the relationship between Pi and cholesterol metabolism has not been clarified. The current study investigated the effects of Npt2a gene ablation that is known as hypophosphatemia model on cholesterol metabolism in mice. Npt2a deficient (Npt2a(-/-)) mice and wild type mice were fed diets with or without 2% cholesterol for 12 days. Plasma lipid and lipoprotein profile analysis revealed that plasma lipid levels (total, LDL and HDL cholesterol) were significantly higher in Npt2a(-/-) mice than wild type (WT) mice. Interestingly, high cholesterol diet markedly increased plasma levels of total, LDL and HDL cholesterol in WT mice, but not Npt2a(-/-) mice. On the other hand, there were no differences in body and liver weight, intake and hepatic lipid accumulation between WT and Npt2a(-/-) mice. These results suggest that ablation of Npt2a gene induces hypercholesterolemia and affects the ability to respond normally to dietary cholesterol. (Keyword) Animals / cholesterol / Cholesterol, Dietary / Female / Hypercholesterolemia / Lipids / Liver / Male / Mice / knockout mice / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa (Tokushima University Institutional Repository) ● Metadata: 106356 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.60.191 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24190035 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887001043 (Tokushima University Institutional Repository: 106356, DOI: 10.2152/jmi.60.191, PubMed: 24190035, Elsevier: Scopus)
35.	Hisami Okumura, T Nakamura-Kutsuzawa, A Teramoto, E Urano, Takafumi Katayama, H Miyake, S Imura, Toru Utsunomiya, M Shimada and Eiji Takeda : Non-esterified fatty acid is being validated as a substitute measure for non-protein respiratory quotient in patients with cirrhosis, e-SPEN Journal, Vol.8, e94, 2013. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clnme.2013.04.003 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84878194782 (DOI: 10.1016/j.clnme.2013.04.003, Elsevier: Scopus)
36.	Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Reply to Letter to the Editor ''On the role of the type III phosphate transporters in vascular calcification'', Bone, Vol.51, No.4, 829, 2012. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2012.07.006 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84865661013 (DOI: 10.1016/j.bone.2012.07.006, Elsevier: Scopus)
37.	Hisami Okumura, Akihiko Kawaura, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Treatment of rapid weight loss in a donor with hepatic steatosis in a living donor liver transplantation: a case report, Hepato-Gastroenterology, Vol.59, No.115, 869-871, 2012. (Summary) The use of steatotic livers for transplantation is often associated with increased primary non-function. To reduce the risk of liver injury, steatosis of the donor liver in living donor liver transplantation (LDLT) was treated with restricted diet and exercise. A 21-year-old male donor, 167cm in height and 87kg in body weight, initially received a 1800kcal/day diet for 9 days which was then gradually reduced using a 1600kcal/day diet for 43 days, followed by a 1500kcal/day diet for one day and was finally maintained on a 1400kcal/day diet for 52 days. Daily exercise consumed 500kcal/day. The non-protein respiratory quotient (npRQ) gradually increased while the non-esterified fatty acids (NEFA) decreased during the course of the 105-day treatment. Consequently, the initial 80% steatosis was reduced to 10% and was accompanied by 13% weight loss for 81 days. The npRQ values and NEFA concentrations in the later period of dietary and exercise treatment were higher and lower, respectively, than in the early treatment period, indicating compensation through long-term treatment. Therefore, energy metabolism and NEFA levels represent important biomarkers for short-term intensive treatment by restricted diet and exercise in donors with hepatic steatosis. (Keyword) Biological Markers / Caloric Restriction / Donor Selection / energy metabolism / Exercise / Fatty Acids, Nonesterified / Fatty Liver / Hepatectomy / Humans / Liver Transplantation / Living Donors / Male / Severity of Illness Index / Time Factors / Treatment Outcome / Weight Loss / Young Adult (Link to Publication Site) ● Publication site (DOI): 10.5754/hge10237 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22469734 ● Search Scopus @ Elsevier (PMID): 22469734 ● Search Scopus @ Elsevier (DOI): 10.5754/hge10237 (DOI: 10.5754/hge10237, PubMed: 22469734)
38.	Akiko Taniguchi-Fukatsu, Hisami Okumura, Yuko Naniwa-Kuroki, Yuka Nishida, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Natto and viscous vegetables in a Japanese style breakfast improved insulin sensitivity, lipid metabolism and oxidative stress in subjects with impaired glucose tolerance, British Journal of Nutrition, Vol.107, No.8, 1184-1191, 2011. (Summary) We previously suggested that the consumption of natto and viscous vegetables as part of a Japanese-style meal based on white rice (WR) reduced postprandial glucose and insulin levels in healthy subjects. The aim of the present study was to assess whether a single breakfast of natto and viscous vegetables or the same breakfast consumed for 2 weeks could improve glucose control, insulin sensitivity, lipid metabolism and oxidative stress in overweight subjects with impaired glucose tolerance (IGT). A total of eleven free-living subjects with IGT followed a randomised, crossover breakfast intervention for 2 weeks. The test meal included boiled WR with natto (viscous fermented soyabeans), Japanese yam and okra. The control meal included WR with non-viscous boiled soyabeans, potatoes and broccoli. Both meals contained comparable amounts of carbohydrate, fat, protein and fibre. The test meal reduced acute glucose and insulin responses compared to the control meal in the study participants. Insulin sensitivity was assessed using the composite insulin sensitivity index (CISI) after both the test and control meal periods. The test meal resulted in improvements in CISI compared to the baseline, whereas no significant changes were observed after the control meal period. Serum levels of both total and LDL-cholesterol were assessed before and after the test meal period and found to decrease significantly. There was also a tendency towards reduced serum malondialdehyde-modified LDL and N( )-carboxymethyllysine. No differences were observed in the measures of chronic glycaemic control. Thus, we conclude that a breakfast of natto and viscous vegetables consumed for 2 weeks improves insulin sensitivity, serum lipid and oxidative stress. (Keyword) Adult / Biological Markers / Cholesterol, LDL / Cross-Over Studies / Female / Glucose Intolerance / Humans / Insulin Resistance / Japan / Lipid Metabolism / Lipids / Male / Malondialdehyde / Middle Aged / Overweight / Oxidative Stress / Soy Foods / Vegetables / Viscosity (Link to Publication Site) ● Publication site (DOI): 10.1017/S0007114511004156 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21899797 ● Search Scopus @ Elsevier (PMID): 21899797 ● Search Scopus @ Elsevier (DOI): 10.1017/S0007114511004156 (DOI: 10.1017/S0007114511004156, PubMed: 21899797)
39.	Takashi Uebanso, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, Sarasa Tanaka, Hidekazu Arai, Yuichiro Takei, Masashi Masuda, Hisami Yamanaka-Okumura and Eiji Takeda : Liver X receptor negatively regulates fibroblast growth factor 21 in the fatty liver induced by cholesterol-enriched diet., The Journal of Nutritional Biochemistry, Vol.23, No.7, 785-790, 2011. (Summary) Cholesterol homeostasis is regulated by the liver X receptor (LXR) at the transcriptional level, but it remains unknown whether LXR can affect expression levels of intrahepatic lipolysis related gene. Recent evidence has demonstrated that fibroblast growth factor 21 (FGF21) regulates hepatic lipolysis and fatty acid utilization. In the present study, we examined the role of LXR in FGF21 gene expression associated with regulation of cross-talk signals between cholesterol and triglyceride metabolism in the liver. An in vivo cholesterol feeding test revealed that intake of excess cholesterol increased cholesterol catabolism related gene expression as well as fatty-acid biosynthesis related gene expression. Moreover, the accumulated cholesterol suppressed FGF21 and hormone-sensitive lipase (HSL) gene expression. After 15-day cholesterol feeding, hepatic triglyceride concentrations were negatively correlated with expression levels of the FGF21 and HSL genes in the liver. An LXR agonist (TO-901317) repressed the FGF21 gene expression in mouse primary hepatocytes and HepG2 cells. A promoter deletion study and electrophoretic mobility shift assay revealed that the human FGF21 promoter has at least one LXR response element located from -37 to -22 bp. In summary, LXR represses FGF21 gene expression at the transcription level and might suppress lipolysis and lipid utilization to protect the liver from excess accumulation of toxic cholesterol. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2011.03.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21889884 ● Search Scopus @ Elsevier (PMID): 21889884 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2011.03.023 (DOI: 10.1016/j.jnutbio.2011.03.023, PubMed: 21889884)
40.	Asuka Shiota, Yutaka Taketani, Yoichi Maekawa, Koji Yasutomo, Masataka Sata, Tohru Sakai, R. Mizuno, M. Isshiki, Hironori Yamamoto and Eiji Takeda : High phosphate diet reduces atherosclerosis formation in apolipoprotein E-deficient mice., Journal of Clinical Biochemistry and Nutrition, Vol.49, No.2, 109-114, 2011. (Summary) Although higher serum phosphate level is a risk factor for cardiovascular diseases in general population as well as chronic kidney disease patients, it has not been clarified whether higher phosphate can affect atherosclerotic plaque formation. In this study, we investigated the effect of prolonged-intake of different concentrations of phosphate on atherosclerosis formation using apolipoprotein E-deficient mice. Apolipoprotein E-deficient mice were fed with high fat diet including 0.6%, 1.2% or 1.8% phosphate. After 20-week treatment, atherosclerotic plaque formation in aorta in 1.8% phosphate diet group was unexpectedly less than that in the other groups. To elucidate mechanisms of suppression of plaque formation by high phosphate diet, we hypothesized that high phosphate diet may modify a profile of monocytes/macrophages suppressing plaque formation. We confirmed that elevated peripheral monocytes (CD11b+, F4/80+ cell numbers) in apolipoprotein E-deficient mice were decreased by feeding with 1.8% P diet. In addition, ex vivo study indicated that high dose of phosphate induced macrophage apoptosis. These observations suggest that excess phosphate intake decreased atherosclerosis formation, at least in part, by changing the profile of peripheral monocytes or inducing apoptosis of macrophages in apolipoprotein E-deficient mice. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.10-150 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21980226 ● Search Scopus @ Elsevier (PMID): 21980226 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.10-150 (DOI: 10.3164/jcbn.10-150, PubMed: 21980226)
41.	Takashi Uebanso, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, Hirokazu Ominami, Hidekazu Arai, Yuichiro Takei, Masashi Masuda, Ayako Tanimura, Nagakatsu Harada, Hisami Yamanaka-Okumura and Eiji Takeda : Paradoxical regulation of human FGF21 by both fasting and feeding signals: is FGF21 a nutritional adaptation factor?, PLoS ONE, Vol.6, No.8, e22976, 2011. (Summary) Fibroblast growth factor 21 (FGF21) has recently emerged as a metabolic hormone involved in regulating glucose and lipid metabolism in mouse, but the regulatory mechanisms and actions of FGF21 in humans remain unclear. Here we have investigated the regulatory mechanisms of the human FGF21 gene at the transcriptional level. A deletion study of the human FGF21 promoter (-1672 to +230 bp) revealed two fasting signals, including peroxisome proliferator-activated receptor α (PPARα) and glucagon signals, that independently induced human FGF21 gene transcription in mouse primary hepatocytes. In addition, two feeding signals, glucose and xylitol, also dose-dependently induced human FGF21 gene transcription and mRNA expression in both human HepG2 cells and mouse primary hepatocytes. FGF21 protein expression and secretion were also induced by high glucose stimulation. The human FGF21 promoter (-1672 to +230 bp) was found to have a carbohydrate-responsive element at -380 to -366 bp, which is distinct from the PPAR response element (PPRE). Knock-down of the carbohydrate response element binding protein by RNAi diminished glucose-induced human FGF21 transcription. Moreover, we found that a region from -555 to -443 bp of the human FGF21 promoter region exerts an important role in the activation of basic transcription. In conclusion, human FGF21 gene expression is paradoxically and independently regulated by both fasting and feeding signals. These regulatory mechanisms suggest that human FGF21 is increased with nutritional crisis, including starvation and overfeeding. (Keyword) Animals / Cell Line / Electrophoretic Mobility Shift Assay / Fasting / Fibroblast Growth Factors / Gene Expression Regulation / Glucose / Humans / Male / Mice / Polymerase Chain Reaction / Promoter Regions, Genetic / Real-Time Polymerase Chain Reaction / Signal Transduction / Xylitol (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0022976 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21829679 ● Search Scopus @ Elsevier (PMID): 21829679 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0022976 (DOI: 10.1371/journal.pone.0022976, PubMed: 21829679)
42.	Kikuko Amou, Hidekazu Arai, Takashi Uebanso, Makiko Fukaya, Megumi Koganei, Hajime Sasaki, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Effects of xylitol on metabolic parameters and visceral fat accumulation., Journal of Clinical Biochemistry and Nutrition, Vol.49, No.1, 1-7, 2011. (Summary) Xylitol is widely used as a sweetener in foods and medications. Xylitol ingestion causes a small blood glucose rise, and it is commonly used as an alternative to high-energy supplements in diabetics. In previous studies, a xylitol metabolite, xylulose-5-phosphate, was shown to activate carbohydrate response element binding protein, and to promote lipogenic enzyme gene transcription in vitro; however, the effects of xylitol in vivo are not understood. Here we investigated the effects of dietary xylitol on lipid metabolism and visceral fat accumulation in rats fed a high-fat diet. Sprague-Dawley rats were fed a high-fat diet containing 0g (control), 1.0g/100kcal (X1) or 2.0g/100kcal (X2) of xylitol. After the 8-week feeding period, visceral fat mass and plasma insulin and lipid concentrations were significantly lower in xylitol-fed rats than those in high-fat diet rats. Gene expression levels of ChREBP and lipogenic enzymes were higher, whereas the expression of sterol regulatory-element binding protein 1c was lower and fatty acid oxidation-related genes were significantly higher in the liver of xylitol-fed rats as compared with high-fat diet rats. In conclusion, intake of xylitol may be beneficial in preventing the development of obesity and metabolic abnormalities in rats with diet-induced obesity. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.10-111 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21765599 ● Search Scopus @ Elsevier (PMID): 21765599 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.10-111 (DOI: 10.3164/jcbn.10-111, PubMed: 21765599)
43.	Jun Shirakawa, Kikuko Amou, Hirokazu Ohminami, Kazuki Orime, Yu Togashi, Yuzuru Ito, Kazuki Tajima, Megumi Koganei, Hajime Sasaki, Eiji Takeda and Yasuo Terauchi : Protective effects of dipeptidyl peptidase-4 (DPP-4) inhibitor against increased cell apoptosis induced by dietary sucrose and linoleic acid in mice with diabetes., The Journal of Biological Chemistry, Vol.286, No.29, 25467-25476, 2011. (Summary) Chronic exposure to high glucose and fatty acid levels caused by dietary sugar and fat intake induces cell apoptosis, leading to the exacerbation of type 2 diabetes. Oleic acid and linoleic acid are two major dietary fatty acids, but their effects in diabetes are unclear. We challenged cell-specific glucokinase haploinsufficient (Gck(+/-)) mice with a diet containing sucrose and oleic acid (SO) or sucrose and linoleic acid (SL) and analyzed cell apoptosis. In Gck(+/-) but not wild-type mice, SL significantly decreased the cell mass and cell proportion in islet cells arising from increased apoptosis to a greater degree than did SO. The mRNA expression of SREBP-1c was significantly higher, and that of E-cadherin was significantly lower in the islets of Gck(+/-) mice fed SL compared with mice fed SO. We next evaluated monotherapy with desfluorositagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, in these mouse groups. DPP-4 inhibitor protected against cell apoptosis, restored the cell mass, and normalized islet morphology in Gck(+/-) mice fed SL. DPP-4 inhibition normalized the changes in the islet expression of SREBP-1c and E-cadherin mRNA induced by the SL diet. Furthermore, linoleic acid induced cell apoptosis to a greater degree in the presence of high glucose levels than in the presence of low glucose levels in vitro in islets and MIN6 cells, whereas a GLP-1 receptor agonist prevented apoptosis. In conclusion, SL exacerbated cell apoptosis in diabetic Gck(+/-) mice but not in euglycemic wild-type mice, and DPP-4 inhibition protected against these effects. (Keyword) Administration, Oral / Animals / apoptosis / Arachidonic Acid / diabetes mellitus / Dietary Carbohydrates / Dipeptidyl Peptidase 4 / Dipeptidyl-Peptidase IV Inhibitors / Dose-Response Relationship, Drug / endoplasmic reticulum / Glucagon-Like Peptide 1 / Glucokinase / glucose / Haploinsufficiency / Insulin-Secreting Cells / Linoleic Acid / Male / Mice / Pyrazines / Receptors, Glucagon / signal transduction / Sucrose / Triazoles (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M110.217216 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21613229 ● Summary page in Scopus @ Elsevier: 2-s2.0-79960387066 (DOI: 10.1074/jbc.M110.217216, PubMed: 21613229, Elsevier: Scopus)
44.	Jun Shirakawa, Hideki Fujii, Kei Ohnuma, Koichiro Sato, Yuzuru Ito, Mitsuyo Kaji, Eri Sakamoto, Megumi Koganei, Hajime Sasaki, Yoji Nagashima, Kikuko Amou, Kazutaka Aoki, Chikao Morimoto, Eiji Takeda and Yasuo Terauchi : Diet-induced adipose tissue inflammation and liver steatosis are prevented by DPP-4 inhibition in diabetic mice., Diabetes, Vol.60, No.4, 1246-1257, 2011. (Summary) Our findings indicated that DPP-4 inhibition has extrapancreatic protective effects against diet-induced adipose tissue inflammation and hepatic steatosis. (Keyword) Adipose Tissue / Animals / Blood Glucose / Body Weight / Chemokine CCL2 / Dietary Fats / Dietary Sucrose / Dipeptidyl Peptidase 4 / Dipeptidyl-Peptidase IV Inhibitors / Enzyme-Linked Immunosorbent Assay / Fatty Liver / Female / Glucokinase / Hypertrophy / insulin / Interferon-gamma / Interleukin-10 / Liver / Male / Mice / Peptides / Polymerase Chain Reaction / Triglycerides / Tumor Necrosis Factor-alpha / Venoms (Link to Publication Site) ● Publication site (DOI): 10.2337/db10-1338 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21330637 ● Summary page in Scopus @ Elsevier: 2-s2.0-79953213304 (DOI: 10.2337/db10-1338, PubMed: 21330637, Elsevier: Scopus)
45.	Ayako Tanimura, Fumiyo Yamada, Akihito Saito, Mikiko Ito, Toru Kimura, Naohiko Anzai, Daisuke Horie, Hironori Yamamoto, Ken-ichi Miyamoto, Yutaka Taketani and Eiji Takeda : Analysis of different complexes of type IIa sodium-dependent phosphate transporter in rat renal cortex using blue-native polyacrylamide gel electrophoresis., The Journal of Medical Investigation : JMI, Vol.58, No.1-2, 140-147, 2011. (Summary) Type IIa sodium-dependent phosphate transporter (NaPi-IIa) can be localized in the apical plasma membrane of renal proximal tubule to carry out a rate-limiting step of phosphate reabsorption. For the apical localization, NaPi-IIa is required to form a macromolecular complex with some adaptor proteins such as Na(+)/H(+) exchanger regulatory factor 1 (NHERF-1) and ezrin. However, the detail of macromolecular complex containing NaPi-IIa in the apical membrane of the renal proximal tubular cells has not been clarified. In this study, we identified at least four different complexes (220, 480, 920, 1,100 kDa) containing NaPi-IIa by using blue-native polyacrylamide gel electrophoresis. Interestingly, LC-MS/MS analysis and immunoprecipitation analysis reveal that megalin is a component of larger complexes (920 and 1,100 kDa). In addition, NaPi-IIa can be heterogeneously co-localized with ezrin and megalin on the apical membrane of renal proximal tubuler cells by fluorescence microscopy analysis. These results suggest that NaPi-IIa can form some different complexes on the apical plasma membrane of renal proximal tubular cells. (Keyword) Animals / Cell Line / Electrophoresis, Gel, Two-Dimensional / Electrophoresis, Polyacrylamide Gel / Kidney Cortex / Kidney Tubules, Proximal / LDL-Receptor Related Protein 2 / Male / Membrane Microdomains / molecular weight / Multiprotein Complexes / Opossums / Protein Interaction Domains and Motifs / Rats / Rats, Sprague-Dawley / Sodium-Phosphate Cotransporter Proteins, Type IIa / Tandem Mass Spectrometry (Tokushima University Institutional Repository) ● Metadata: 82750 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.58.140 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372499 ● Search Scopus @ Elsevier (PMID): 21372499 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.140 (Tokushima University Institutional Repository: 82750, DOI: 10.2152/jmi.58.140, PubMed: 21372499)
46.	Hisami Okumura, 浦野恵利, 板東友美, 山内利香, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Nutritional Assessment of Pre- and Post- Liver Resection by Energy Metabolism and Laboratory Data, Journal of Japanese Society of Clinical Nutrition, Vol.32, No.3, 133-140, 2011. (Keyword) liver resection / indirect calorimetry / non-protein respiratory quotient (npRQ) / non-esterified fatty acids (NEFA) / 遊離脂肪酸 / NEFA / liver resection / indirect calorimetry / non-protein respiratory quotient / non-esterified fatty acids (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520853832562768896 (CiNii: 1520853832562768896)
47.	Rie Mukai, Reiko Nakao, Hironori Yamamoto, Takeshi Nikawa, Eiji Takeda and Junji Terao : Quercetin Prevents Unloading-Derived Disused Muscle Atrophy by Attenuating the Induction of Ubiquitin Ligases in Tail-Suspension Mice., Journal of Natural Products, Vol.73, No.10, 1708-1710, 2010. (Summary) The effects of quercetin (1) were investigated on disused muscle atrophy using mice that underwent tail suspension. Periodic injection of 1 into the gastrocnemius muscle suppressed muscle weight loss and ubiquitin ligase expression. Compound 1 reduced the enhancement of lipid peroxidation in the muscle. Injection of N-acetyl-l-cysteine, but not flavone (2), also prevented muscle weight loss and enhancement of lipid peroxidation. These findings demonstrate that 1 can prevent disused muscle atrophy by attenuating the expression of ubiquitin ligases and that such prevention originates from its antioxidant activity. (Link to Publication Site) ● Publication site (DOI): 10.1021/np100240y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20853873 ● Search Scopus @ Elsevier (PMID): 20853873 ● Search Scopus @ Elsevier (DOI): 10.1021/np100240y (DOI: 10.1021/np100240y, PubMed: 20853873)
48.	Satoru Imura, Mitsuo Shimada, Toru Utsunomiya, Yuji Morine, Tetsuya Ikemoto, Hiroki Mori, Jun Hanaoka, Shuichi Iwahashi, Yu Saito, Hisami Okumura and Eiji Takeda : Impact of splenectomy in patients with liver cirrhosis: Results from 18 patients in a single center experience., Hepatology Research, Vol.40, No.9, 894-900, 2010. (Summary) Aim: With the recent advances in medical or surgical treatments in chronic hepatic disorders, the indications for splenectomy in hepatic disorders have greatly expanded. We performed splenectomy for cirrhotic patients and investigated the effects of splenectomy on hepatic functional reserve and nutrition metabolism. Methods: Eighteen patients (Child-Pugh B/C: 12/6; Child-Pugh A: excluded) who underwent splenectomy at our institute between 2005 and 2008 were enrolled. Twelve patients (67%) had hepatocellular carcinoma (HCC), eight of whom met the Milan criteria. Results: Overall survival rate was 83.3% at 1 year and 62.7% at 2 years. The survival rate of six patients with liver cirrhosis classified a Child-Pugh C was 80.0% at 1 year and 60.0% at 2 years. Three patients underwent hepatic resection and nine patients received ablation therapy against hepatocelluar carcinoma. Portal pressure decreased after splenectomy in most patients (mean decrease, 4.7 mmHg). Four weeks after the operation, the markers of hepatic functional reserve, indocyanine green retention rate at 15 min (ICGR15) and Technetium-99m-galactosyl human serum albumin value ((99m)Tc-GSA), improved from 38.5% to 35.1% and from 0.773 to 0.788 (LHL15), respectively. The non-protein respiratory quotient (npRQ) did not change in short period after the operation. Other outcomes, including liver function test in cirrhotic patients with long-term (1 year) follow-up after splenectomy (n = 7), did not improve significantly. Post-operative complications included portal thrombus (n = 2), ascites (n = 2) were observed in six patients (33%). Conclusion: Splenectomy improved hepatic functional reserve and nutritional metabolism in some cases. However, the long-term outcomes should still be evaluated. (Keyword) 欧文論文 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1872-034X.2010.00688.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20887594 ● Search Scopus @ Elsevier (PMID): 20887594 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1872-034X.2010.00688.x (DOI: 10.1111/j.1872-034X.2010.00688.x, PubMed: 20887594)
49.	Asuka Shiota, Takahiko Hada, Tomoko Baba, Minako Sato, Hisami Okumura, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Protective effects of glycoglycerolipids extracted from spinach on 5-fluorouracil induced intestinal mucosal injury., The Journal of Medical Investigation : JMI, Vol.57, No.3-4, 314-320, 2010. (Summary) Glycoglycerolipids are mostly found in plants, however the beneficial effects of the glycoglycerolipids on mammalian body have not been understood. In this study, we investigated the effects of glycolipid extracts from spinach, which highly contained glycoglycerolipids, on mucosal injury induced by 5-fluorouracil (5-FU) in rats. Preadministration of glycolipid extracts from spinach (20 mg/kg body weight) prevented villous atrophy, misaligned crypts, and increased inflammatory cytokines in rat jejunum treated with 5-FU (300 mg/kg body weight) compared with the extracts from soybean. The glycolipid extracts from spinach highly contained monogalactosyl-diacylglycerol (MGDG) and diglactosyl-diacylglycerol (DGDG). In Caco-2 cells, MGDG and DGDG inhibited the production of reactive oxygen species induced by phorbol ester. We concluded that glycolipid extracts from spinach has anti-oxidative and anti-inflammatory effects, and the extract may be useful for prevention of drug-induced mucosal injury and other inflammatory diseases. Tokushima (Keyword) Alkaline Phosphatase / Animals / Anti-Inflammatory Agents, Non-Steroidal / Antioxidants / Caco-2 Cells / Cytokines / Fluorouracil / Galactolipids / Glycolipids / Humans / Intestinal Mucosa / Male / Mucositis / Plant Extracts / RNA, Messenger / Rats / Rats, Sprague-Dawley / reactive oxygen species / Soybeans / Spinacia oleracea (Tokushima University Institutional Repository) ● Metadata: 79153 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.57.314 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20847532 ● Summary page in Scopus @ Elsevier: 2-s2.0-78649650737 (Tokushima University Institutional Repository: 79153, DOI: 10.2152/jmi.57.314, PubMed: 20847532, Elsevier: Scopus)
50.	Hiroaki Yanagawa, Junji Terao, Eiji Takeda, Yoshihisa Takaishi, Yoshiki Kashiwada, Kazuyoshi Kawazoe, Fushitani Shuji, Koichiro Tsuchiya, Aiko Yamauchi, Sato Chiho and Minoru Irahara : Consultation clinics for complementary and alternative medicine at Japanese university hospitals: An analysis at Tokushima University Hospital, Experimental and Therapeutic Medicine, Vol.1, No.3, 481-483, 2010. (Summary) Here, we report on a Consultation Clinic for Complementary and Alternative Medicine (CAM) which we established at Tokushima University Hospital in July of 2007 with the aim of providing person-to-person information on CAM, though not CAM therapy itself. In December of 2008, we received 55 applications for consultation, 37% concerning health foods, 37% Japanese herbal medicine (Kampo), and 26% various other topics. The consultants (nutritionists and pharmacists) communicated individually with 38 applicants; malignancies (26%) and cardiovascular disease (24%) were the main underlying concerns. To promote the quality of consultation, data was collected by means of focus group interviews concerning the perspective of the consultants. Safe and effective use of CAM requires a network of communication linking individuals, consultation teams, physicians, primary care institutions and university hospitals. To advance this goal, we plan to broaden the efforts described herein. Our findings indicate that the specific role of the consultation clinic in promoting the scientific use of CAM merits further study. (Link to Publication Site) ● Publication site (DOI): 10.3892/etm_00000075 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22993564 ● Search Scopus @ Elsevier (PMID): 22993564 ● Search Scopus @ Elsevier (DOI): 10.3892/etm_00000075 (DOI: 10.3892/etm_00000075, PubMed: 22993564)
51.	Hisami Okumura, Taki Nakamura, Hidenori Miyake, Harumi Takeuchi, Takafumi Katayama, Yuji Morine, Satoru Imura, Mitsuo Shimada and Eiji Takeda : Effect of long-term late-evening snack on health-related quality of life in cirrhotic patients., Hepatology Research, Vol.40, No.5, 470-476, 2010. (Summary) Aim: In patients with liver cirrhosis, abnormal energy metabolism induces low health-related quality of life (HRQOL) scores. However, late-evening snack (LES) prevents morning starvation in cirrhotic patients. Our aim is to assess the effect of long-term LES on HRQOL in cirrhotic patients, using the 36-item Short Form (SF-36) health survey. Methods: Thirty-nine cirrhotic patients classified as Child-Pugh grade A were recruited. The patients were randomly divided into two groups: 24 were assigned to the non-LES group and 15 to the LES group. SF-36 scores, anthropometric data and serum biochemical parameters were examined in the non-LES and LES groups at 0, 6 and 12 months. Results: Neither anthropometric data nor laboratory data showed significant differences between the non-LES and the LES groups at 0, 6 and 12 months. The role-emotional (RE) HRQOL scores at 6 months and mental health (MH) scores at 6 and 12 months were significantly reduced from the baseline level in the non-LES group. In contrast, these scores remained unchanged in the LES group. General health perception (GH) scores at 12 months, RE at 6 months and MH at 6 and 12 months in the LES group were significantly higher than those of the non-LES group. Conclusion: Long-term LES administration may be helpful in maintaining higher HRQOL in patients with cirrhosis. (Keyword) 欧文論文 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1872-034X.2010.00637.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20412329 ● Search Scopus @ Elsevier (PMID): 20412329 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1872-034X.2010.00637.x (DOI: 10.1111/j.1872-034X.2010.00637.x, PubMed: 20412329)
52.	Mariko Ishiguro, Hironori Yamamoto, Masashi Masuda, Mina Kozai, Yuichiro Takei, Sarasa Tanaka, Tadatoshi Sato, Hiroko Segawa, Yutaka Taketani, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Thyroid hormones regulate phosphate homoeostasis through transcriptional control of the renal type IIa sodium-dependent phosphate co-transporter (Npt2a) gene., The Biochemical Journal, Vol.427, No.1, 161-169, 2010. (Summary) The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. It has been demonstrated previously that renal Npt2a protein and its mRNA expression are both up-regulated by the thyroid hormone T3 (3,3',5-tri-iodothyronine) in rats. However, it has never been established whether the induction was mediated by a direct effect of thyroid hormones on the Npt2a promoter. To address the role of Npt2a in T3-dependent regulation of phosphate homoeostasis and to identify the molecular mechanisms by which thyroid hormones modulate Npt2a gene expression, mice were rendered pharmacologically hypo- and hyper-thyroid. Hypothyroid mice showed low levels of serum phosphate and a marked decrease in renal Npt2a protein abundance. Importantly, we also showed that Npt2a-deficient mice had impaired serum phosphate responsiveness to T3 compared with wild-type mice. Promoter analysis with a luciferase assay revealed that the transcriptional activity of a reporter gene containing the Npt2a promoter and intron 1 was dependent upon TRs (thyroid hormone receptors) and specifically increased by T3 in renal cells. Deletion analysis and EMSAs (electrophoretic mobility-shift assays) determined that there were unique TREs (thyroid-hormone-responsive elements) within intron 1 of the Npt2a gene. These results suggest that Npt2a plays a critical role as a T3-target gene, to control phosphate homoeostasis, and that T3 transcriptionally activates the Npt2a gene via TRs in a renal cell-specific manner. (Keyword) Animals / COS Cells / Cercopithecus aethiops / Dogs / Electrophoretic Mobility Shift Assay / Female / Gene Expression Regulation / Hela Cells / homeostasis / Humans / Kidney / Luciferases / Male / Mice / Mice, Knockout / Phosphates / Promoter Regions, Genetic / Rats / Receptors, Thyroid Hormone / Response Elements / Sodium-Phosphate Cotransporter Proteins, Type IIa / Transcription, Genetic / Transcriptional Activation / Triiodothyronine (Link to Publication Site) ● Publication site (DOI): 10.1042/BJ20090671 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20088828 ● Summary page in Scopus @ Elsevier: 2-s2.0-77950874525 (DOI: 10.1042/BJ20090671, PubMed: 20088828, Elsevier: Scopus)
53.	Hidekazu Arai, Naomi Awane, Akira Mizuno, Makiko Fukaya, Masae Sakuma, Nagakatsu Harada, Akihiko Kawaura, Hironori Yamamoto, Hisami Okumura, Yutaka Taketani, Toshio Doi and Eiji Takeda : Increasing early insulin secretion compensate adequately for hepatic insulin resistance in CCl4-induced cirrhosis rats., The Journal of Medical Investigation : JMI, Vol.57, No.1-2, 54-61, 2010. (Summary) A number of recent publications have reported an increased frequency prevalence of glucose intolerance with hyperinsulinemia in liver cirrhosis. The aim of this work was to detect, in CCl(4)-induced liver cirrhosis rat, the presence and starting point of muscle and liver insulin resistance. Eighteen rats received intraperitoneal injection of 2 ml of soybean oil containing of CCl(4) twice a week for 20 weeks. We executed standard oral glucose tolerance and clamp study to evaluate systemic insulin resistance. Hepatic glucose uptake was much lower in CCl(4) group than that in control group, but peripheral glucose uptake was not decreased in this study. In contrast, early-phase insulin secretion was enhanced in CCl(4) rat using oral glucose load during clamp methods. These data suggested that increased early insulin secretion compensate adequately for hepatic insulin resistance in rats. However there was a report that peripheral glucose uptake was decreased in the case of human liver cirrhosis, which was formed in the course of time. In a chronic condition, this may be associated with reduced insulin content and developed systemic insulin resistance in liver cirrhosis. Then a long term observation study will be required to examine the presence of muscle insulin resistance in liver cirrhosis. (Keyword) Animals / Body Weight / carbon tetrachloride / glucose / insulin / insulin resistance / Liver / Liver Cirrhosis, Experimental / Male / Organ Size / Rats / Rats, Sprague-Dawley (Tokushima University Institutional Repository) ● Metadata: 77532 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.57.54 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20299743 ● Search Scopus @ Elsevier (PMID): 20299743 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.57.54 (Tokushima University Institutional Repository: 77532, DOI: 10.2152/jmi.57.54, PubMed: 20299743)
54.	Takashi Uebanso, Yutaka Taketani, Makiko Fukaya, Kazusa Sato, Yuichiro Takei, Tadatoshi Sato, Naoki Sawada, Kikuko Amou, Nagakatsu Harada, Hidekazu Arai, Hironori Yamamoto and Eiji Takeda : Hypocaloric high protein diet improves fatty liver and hypertriglyceridemia in sucrose-fed obese rats via two pathways., American Journal of Physiology, Endocrinology and Metabolism, Vol.297, No.1, 76-84, 2009. (Summary) The mechanism by which replacement of some dietary carbohydrates with protein during weight loss favors lipid metabolism remains obscure. In this study, we investigated the effect of an energy-restricted, high-protein/low-carbohydrate diet on lipid metabolism in obese rats. High-sucrose-induced obese rats were assigned randomly to one of two energy-restricted dietary interventions: a carbohydrate-based control diet (CD) or a high-protein diet (HPD). Lean rats of the same age were assigned as normal control. There was significantly greater improvement in fatty liver and hypertriglyceridemia with the HPD diet relative to the CD diet. Expression of genes regulated by fibroblast growth factor-21 (FGF21) and involved in liver lipolysis and lipid utilitization, such as lipase and acyl-CoA oxidase, increased in obese rats fed the HPD. Furthermore, there was an inverse correlation between levels of FGF21 gene expression (regulated by glucagon/insulin balance) and increased triglyceride concentrations in liver from obese rats. Expression of hepatic stearoyl-CoA desaturase-1 (SCD1), regulated primarily by the dietary carbohydrate, was also markedly reduced in the HPD group (similar to plasma triglyceride levels in fasting animals) relative to the CD group. In conclusion, a hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia effectively relative to a carbohydrate diet. The two cellular pathways at work behind these benefits include stimulation of hepatic lipolysis and lipid utilization mediated by FGF21 and reduction of hepatic VLDL-TG production by SCD1 regulation. (Keyword) Animals / Blood Glucose / Caloric Restriction / Cells, Cultured / Diet, Reducing / Dietary Proteins / Fasting / Fatty Liver / Feeding Behavior / Hypertriglyceridemia / Male / obesity / Rats / Rats, Sprague-Dawley / signal transduction / Sucrose (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00014.2009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19435858 ● Search Scopus @ Elsevier (PMID): 19435858 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00014.2009 (DOI: 10.1152/ajpendo.00014.2009, PubMed: 19435858)
55.	Emi Shuto, Yutaka Taketani, Tanaka Rieko, Nagakatsu Harada, Isshiki Masashi, Sato Minato, Nashiki Kunitaka, Amo Kikuko, Hironori Yamamoto, Higashi Yukihito, Yutaka Nakaya and Eiji Takeda : Dietary Phosphorus Acutely Impairs Endothelial Function., Journal of the American Society of Nephrology, Vol.20, No.7, 1504-1512, 2009. (Summary) Excessive dietary phosphorus may increase cardiovascular risk in healthy individuals as well as in patients with chronic kidney disease, but the mechanisms underlying this risk are not completely understood. To determine whether postprandial hyperphosphatemia may promote endothelial dysfunction, we investigated the acute effect of phosphorus loading on endothelial function in vitro and in vivo. Exposing bovine aortic endothelial cells to a phosphorus load increased production of reactive oxygen species, which depended on phosphorus influx via sodium-dependent phosphate transporters, and decreased nitric oxide production via inhibitory phosphorylation of endothelial nitric oxide synthase. Phosphorus loading inhibited endothelium-dependent vasodilation of rat aortic rings. In 11 healthy men, we alternately served meals containing 400 mg or 1200 mg of phosphorus in a double-blind crossover study and measured flow-mediated dilation of the brachial artery before and 2 h after the meals. The high dietary phosphorus load increased serum phosphorus at 2 h and significantly decreased flow-mediated dilation. Flow-mediated dilation correlated inversely with serum phosphorus. Taken together, these findings suggest that endothelial dysfunction mediated by acute postprandial hyperphosphatemia may contribute to the relationship between serum phosphorus level and the risk for cardiovascular morbidity and mortality. (Link to Publication Site) ● Publication site (DOI): 10.1681/ASN.2008101106 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19406976 ● Search Scopus @ Elsevier (PMID): 19406976 ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.2008101106 (DOI: 10.1681/ASN.2008101106, PubMed: 19406976)
56.	鶴尾美穂, 寺沢敏秀, Hisami Okumura and Eiji Takeda : 超速効型インスリン注射と就寝前夜食療法を併用した肝硬変合併糖尿病の4症例, The Journal of Metabolism and Clinical Nutrition, Vol.12, No.1, 51-57, 2009. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572824499876024704 (CiNii: 1572824499876024704)
57.	Kazuyoshi Kitaoka, Kaoru Uchida, Naoko Okamoto, Sachiko Chikahisa, Toshitsugu Miyazaki, Eiji Takeda and Hiroyoshi Sei : Fermented ginseng improves the first-night effect in humans, Sleep, Vol.32, No.3, 413-421, 2009. (Summary) The goal of this study was to clarify whether ginseng fermented by lactic acid bacteria (fermented ginseng, FG), can improve the first-night effect (FNE) in humans. Behavioral tests and quantification of mRNA expression related to GABAergic neurotransmission in brain (glutamic acid decarboxylase 1, gamma-aminobutyrate aminotransferase [Abat], gamma-aminobutyric acid transporter 1 [GAT1], gamma-aminobutyric acid transporter 4, gamma-aminobutyric acid A receptor subunit alpha 1 and gamma-aminobutyric acid A receptor subunit alpha 2) were carried out in FG-treated mice. We also performed double-blind sleep recordings of human subjects given FG or placebo. A university-based sleep laboratory. Sixteen healthy male volunteers (aged 20.69 +/- 0.44 years) were observed in the human study. At the end of administration, 2 consecutive all-night polysomnography recordings were performed. Subjects also completed psychological questionnaires, and urine and saliva samples were taken to analyze stress-sensitive markers. The light-dark transition test demonstrated that FG had some anxiolytic effect in mice, but other anxiety measures were unaffected. The hippocampal mRNA expression showed a decrease of Abat and GAT1 suggesting an increase of GABA. Other regions (amygdala and cerebellum) showed no differences. Furthermore, there was some evidence (using simple pairwise comparisons but not supported in the full ANOVA model) that administration of FG tended to diminish decreases in total sleep time and sleep efficiency (seen as first night effects in the placebo group) without affecting sleep architecture. Our results suggest the administration of FG could improve the FNE in humans. The improvement may be related to an anxiolytic effect of FG which acts via GABAergic modification. (Keyword) sleep (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19294962 ● Search Scopus @ Elsevier (PMID): 19294962 (PubMed: 19294962)
58.	Masae Sakuma, Hisami Okumura, Yuko Naniwa, Dai Matsumoto, Megumi Tsunematsu, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Dose-dependent effects of barley cooked with white rice on postprandial glucose and desacyl ghrelin levels., Journal of Clinical Biochemistry and Nutrition, Vol.44, No.2, 151-159, 2009. (Summary) White rice is an indispensable staple food in Japan, although it is a high glycemic index food. The objective of this study was to estimate how barley cooked with white rice might affect postprandial glucose, insulin and desacyl ghrelin concentrations as well as fullness. The study was conducted in randomized crossover design with nine healthy subjects. Blood glucose, insulin, free fatty acid and desacyl ghrelin concentrations and subjective levels of fullness and hunger were measured for 240 min after intake of glucose, white rice, 30% rolled barley (30BAR), 50% rolled barley (50BAR) and 100% rolled barley (100BAR) containing 75 g of available carbohydrate. Postprandial glucose and insulin levels were suppressed by intake of 30BAR, 50BAR and 100BAR comparing with those of white rice. Area under the curves of plasma glucose and insulin concentrations was reduced by barley intake in a dose-dependent manner. Although plasma desacyl ghrelin levels decreased postprandially, the degree of reduction was suppressed by barley intake in a dose-dependent manner. Postprandial desacyl ghrelin levels can be a sensitive biomarker of carbohydrate metabolism. The combination of white rice with barley plays a beneficial role in preventing and treating type 2 diabetes, obesity and other metabolic diseases. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.08-232 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19308269 ● Search Scopus @ Elsevier (PMID): 19308269 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.08-232 (DOI: 10.3164/jcbn.08-232, PubMed: 19308269)
59.	Yuichiro Takei, Hironori Yamamoto, Masashi Masuda, Tadatoshi Sato, Yutaka Taketani and Eiji Takeda : Stanniocalcin 2 is positively and negatively controlled by 1,25(OH)(2)D(3) and PTH in renal proximal tubular cells., Journal of Molecular Endocrinology, Vol.42, No.3, 261-268, 2009. (Summary) We have previously identified a second mammalian stanniocalcin (STC2) in humans and demonstrated that STC2 inhibits phosphate uptake in an opossum renal proximal tubular cell line (opossum kidney (OK) cells). However, the regulation of Stc2 gene expression in OK cells is not well understood. In this study, we identified the opossum Stc2 cDNA sequence. The opossum STC2 amino acid sequence had 78.8% homology with human STC2, and has a conserved putative N-linked glycosylation site. Next, we investigated the regulation of Stc2 gene expression by the classical calcium and phosphate-regulating factors 1,25(OH)(2)D(3) and PTH in OK cells. In western blot analysis using affinity-purified anti-STC2 antibody, the secretion of STC2 protein was stimulated by 1,25(OH)(2)D(3) in a dose-dependent manner. By contrast, PTH suppressed the induction of STC2 protein secretion by 1,25(OH)(2)D(3). Real-time PCR analysis revealed that Stc2 mRNA expression was increased by 1,25(OH)(2)D(3) in a dose- and time-dependent manner. In addition, actinomycin D, an RNA synthesis inhibitor, prevented the effects of 1,25(OH)(2)D(3) on Stc2 gene expression. On the other hand, PTH and phorbol 12,13-myristic acetate, a specific PKC activator, but not 8-bromo-cyclic AMP, a specific PKA activator, reduced the mRNA levels of Stc2. In addition, Gö6976, a specific PKC inhibitor, abolished the downregulation of Stc2 mRNA expression by PTH. Furthermore, we demonstrated that the renal Stc2 mRNA expression was increased by 1,25(OH)(2)D(3) and decreased by PTH in vivo. These results suggest that STC2 is positively and negatively controlled by 1,25(OH)(2)D(3) and PTH in renal proximal tubular cells. (Keyword) Amino Acid Sequence / Animals / Blotting, Western / Calcitriol / Calcium Channel Agonists / Cell Line / Gene Expression Regulation / Glycoproteins / Humans / Immunohistochemistry / Intercellular Signaling Peptides and Proteins / Kidney Tubules, Proximal / Molecular Sequence Data / Opossums / Parathyroid Hormone / Reverse Transcriptase Polymerase Chain Reaction / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1677/JME-08-0161 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19131501 ● Search Scopus @ Elsevier (PMID): 19131501 ● Search Scopus @ Elsevier (DOI): 10.1677/JME-08-0161 (DOI: 10.1677/JME-08-0161, PubMed: 19131501)
60.	Hisami Okumura, 廣瀬美和, Eiji Takeda, Masaaki Uno and Shinji Nagahiro : NST症例におけるワルファリン治療に及ぼす経腸栄養剤のビタミンK含有量の影響の検討, Nutrition Support Journal, Vol.10, No.1, 27-30, 2009.
61.	Emi Shuto, Yutaka Taketani, Tohru Sakai and Eiji Takeda : Hyperphosphatemia and cardiovascular disease, Shikoku Acta Medica, Vol.64, No.3,4, 114-116, 2008. (Summary) Hyperphosphatemia has been known as a risk factor for cardiovascular disease particularly inchronic kidney disease patients. Hyperphosphatemia can be involved in the calcification of vascularsmooth muscle cells, resulting in M¨onkeberg medial calcific sclerosis which is a type of arteriosclerosis.However, it has not been clarified whether hyperphosphatemia can deteriorate endothelialfunction and can be a risk factor of atherosclerosis. Our recent study demonstrated that hyperphosphatemiaincreased oxidative stress and decreased nitric oxide production in endothelial cells.In addition, hyperphosphatemia attenuated endothelium-dependent vasodilation reaction. Theseobservations suggest that hyperphosphatemia may cause endothelial dysfunction, and be an importantfactor for progression of atherosclerosis as well as vascular calcification. Positive associationbetween hyperphosphatemia and cardiovascular disease may be explained by the dual harmfuleffects of phosphorus on the vessels. (Keyword) hyperphosphatemia / cardiovascular disease / endothelial cell / oxidative stress / vascular calcification (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287418501888 (CiNii: 1050564287418501888)
62.	Kazusa Sato, Hidekazu Arai, Yui Miyazawa, Makiko Fukaya, Takashi Uebanso, Megumi Koganei, Hajime Sasaki, Tadatoshi Sato, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Palatinose and oleic acid act together to prevent pancreatic islet disruption in nondiabetic obese Zucker rats., The Journal of Medical Investigation : JMI, Vol.55, No.3-4, 183-195, 2008. (Summary) We showed previously that 8-wk consumption of a diet containing palatinose (P, a slowly-absorbed sucrose analogue) and oleic acid (O) ameliorates but a diet containing sucrose (S) and linoleic acid (L) aggravates metabolic abnormalities in Zucker fatty (fa/fa) rats. In this study, we aimed to identify early changes in metabolism in rats induced by certain combinations of carbohydrates and fatty acids. Specifically, male Zucker fatty rats were fed an isocaloric diet containing various combinations of carbohydrates (P; S) and fatty acids (O; L). After 4 wk, no significant differences in body weight, visceral fat mass, plasma parameters (glucose, insulin, lipids, and adipokines), hepatic adiposity and gene expression, and adipose inflammation were observed between dietary groups. In contrast, pancreatic islets of palatinose-fed (PO and PL) rats were smaller and less fibrotic than sucrose-fed (SO and SL) rats. The abnormal alpha-cell distribution and sporadic staining of active caspase-3 common to islets of linoleic-acid-fed rats were not observed in oleic-acid-fed (PO and SO) rats. Accordingly, progressive beta-cell loss was seen in SL rats, but not in PO rats. These findings suggest that pancreatic islets may be initial sites that translate the effects of different combinations of dietary carbohydrates and fats into metabolic changes. (Keyword) Adipocytes / Animals / apoptosis / Base Sequence / DNA Primers / Dietary Carbohydrates / Dietary Fats, Unsaturated / Disease Models, Animal / Fibrosis / Humans / Islets of Langerhans / Isomaltose / Male / Metabolic Syndrome X / obesity / Oleic Acid / Rats / Rats, Zucker / Sucrose (Tokushima University Institutional Repository) ● Metadata: 110858 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.55.183 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18797130 ● Search Scopus @ Elsevier (PMID): 18797130 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.55.183 (Tokushima University Institutional Repository: 110858, DOI: 10.2152/jmi.55.183, PubMed: 18797130)
63.	Yuko Shiba, Takashi Kinoshita, Hiroshi Chuman, Yutaka Taketani, Eiji Takeda, Yoji Kato, Michitaka Naito, Kyuichi Kawabata, Akari Ishisaka, Junji Terao and Yoshichika Kawai : Flavonoids as Substrates and Inhibitors of Myeloperoxidase : Molecular Actions of Aglycone and Metabolites, Chemical Research in Toxicology, Vol.21, No.8, 1600-1609, 2008. (Summary) Myeloperoxidase (MPO), secreted by activated neutrophils and macrophages at the site of inflammation, may be implicated in the oxidation of protein/lipoprotein during the development of cardiovascular diseases. Flavonoids have been suggested to act as antioxidative and anti-inflammatory agents in vivo; however, their molecular actions have not yet been fully understood. In this study, we examined the molecular basis of the inhibitory effects of dietary flavonoids, such as quercetin, and their metabolites on the catalytic reaction of MPO using a combination of biological assays and theoretical calculation studies. Immunohistochemical staining showed that a quercetin metabolite was colocalized with macrophages, MPO, and dityrosine, an MPO-derived oxidation product of tyrosine, in human atherosclerotic aorta. Quercetin and the plasma metabolites inhibited the formation of dityrosine catalyzed by the MPO enzyme and HL-60 cells in a dose-dependent manner. Spectrometric analysis indicated that quercetin might act as a cosubstrate of MPO resulting in the formation of the oxidized quercetin. Quantitative structure-activity relationship studies showed that the inhibitory actions of flavonoids strongly depended not only on radical scavenging activity but also on hydrophobicity (log P). The requirement of a set of hydroxyl groups at the 3, 5, and 4'-positions and C2-C3 double bond was suggested for the inhibitory effect. The binding of quercetin and the metabolites to a hydrophobic region at the entrance to the distal heme pocket of MPO was also proposed by a computer docking simulation. The current study provides the structure-activity relationships for flavonoids as the anti-inflammatory dietary constituents targeting the MPO-derived oxidative reactions in vivo. (Keyword) Administration, Oral / Animals / Antioxidants / Aorta / atherosclerosis / Computer Simulation / Dose-Response Relationship, Drug / Enzyme Inhibitors / Free Radical Scavengers / HL-60 Cells / Humans / Macrophages / Peroxidase / Quantitative Structure-Activity Relationship / Quercetin / Rats / Rats, Inbred Strains / Tyrosine (Link to Publication Site) ● Publication site (DOI): 10.1021/tx8000835 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18620432 ● Search Scopus @ Elsevier (PMID): 18620432 ● Search Scopus @ Elsevier (DOI): 10.1021/tx8000835 (DOI: 10.1021/tx8000835, PubMed: 18620432)
64.	Hiroyoshi Sei, Katsutaka Oishi, Sachiko Chikahisa, Kazuyoshi Kitaoka, Eiji Takeda and Norio Ishida : Diurnal amplitudes of arterial pressure and heart rate are dampened in Clock mutant mice and adrenalectomized mice., Endocrinology, Vol.149, No.7, 3576-3580, 2008. (Summary) Arterial pressure (AP), heart rate (HR), and cardiovascular diseases, including ischemic heart attack and cerebrovascular accident, show diurnal variation. Evidence that circadian-related genes contribute to cardiovascular control has been accumulated. In this study, we measured the AP and HR of Clock mutant mice on the Jcl/ICR background to determine the role of the Clock gene in cardiovascular function. Mice with mutated Clock genes had a dampened diurnal rhythm of AP and HR, compared with wild-type control mice, and this difference disappeared after adrenalectomy. The diurnal acrophase in both mean arterial pressure and HR was delayed significantly in Clock mutant mice, compared with wild-type mice, and this difference remained after adrenalectomy. Clock mutant mice had a lower concentration of plasma aldosterone, compared with wild-type mice. Our data suggest that the adrenal gland is involved in the diurnal amplitude, but not the acrophase, of AP and HR, and that the function of the Clock gene may be related to the nondipping type of AP elevation. (Keyword) Adrenalectomy / Animals / Blood Pressure / Circadian Rhythm / Female / Genotype / Heart Rate / Male / Mice / Mice, Inbred BALB C / Mice, Inbred C57BL / Mice, Inbred ICR / Mice, Mutant Strains / Mutation / Trans-Activators (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2007-1714 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18403480 ● Search Scopus @ Elsevier (PMID): 18403480 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2007-1714 (DOI: 10.1210/en.2007-1714, PubMed: 18403480)
65.	Kyoko Yuasa, Masako Sei, Eiji Takeda, ASHRAF ABDEL AZIM EWIS, Hokuma Munakata, Chiemi Onishi and Yutaka Nakahori : Effects of lifestyle habits and eating meals together with the family on the prevalence of obesity among school children in Tokushima, Japan: a cross-sectional questionnaire-based survey., The Journal of Medical Investigation : JMI, Vol.55, No.1-2, 71-77, 2008. (Summary) Obesity in children has become a major global public health concern. The prevention of obesity must start from early childhood in order to establish sound lifestyle habits and promote healthy adulthood. In this study, we evaluated factors associated with the prevention of obesity and the development of healthy lifestyle habits in children. A cross-sectional, questionnaire-based survey was performed in elementary and junior high school students in Tokushima Prefecture, Japan, during the summer of 2004. The questionnaire consisted of 30 items such as physique, sleep, eating habits, diet, exercise, free time, and attending after-school lessons. Our study revealed that eating meals as a family every day is associated with a lower rate of obesity as well as getting good lifestyle habits such as eating balanced meals and getting enough sleep. Of the 3,291 students who responded to the questionnaire, 2,688 (81.7%) reported that they eat meals with their family every day. The percentage of students who eat meals with their family every day decreased with increasing school grade, with the lowest percent in the junior high school students. However, the results regarding female junior high school students revealed a marked association between eating meals with the family every day and good lifestyle habits. We recommend that parents and school teaching staff encourage the establishment of sound, healthy lifestyle habits in children from early childhood as an effective measure for the prevention of obesity. (Keyword) Adolescent / children / Cross-Sectional Studies / family / Feeding Behavior / Japan / lifestyle / obesity (Tokushima University Institutional Repository) ● Metadata: 110841 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.55.71 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18319548 ● Summary page in Scopus @ Elsevier: 2-s2.0-43149118763 (Tokushima University Institutional Repository: 110841, DOI: 10.2152/jmi.55.71, PubMed: 18319548, Elsevier: Scopus)
66.	Akiko Taniguchi, Hisami Okumura, Yuka Nishida, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Natto and viscous vegetables in a Japanese style meal suppress postprandial glucose and insulin responses, Asia Pacific Journal of Clinical Nutrition, Vol.17, No.4, 663-668, 2008. (Summary) Naturally viscous vegetables and natto, made by fermenting soybeans, are very palatable and considered to be healthy foods in Japan. The objective was to assess whether the consumption of natto and viscous vegetables as part of a traditional Japanese breakfast based on high-glycemic index white rice affects glycemic, insulinemic, lipidemic and satiety responses in healthy subjects. Eleven healthy subjects consumed the reference, control and test meals in a randomized cross-over design. The test meal, comprising 200 g of boiled white rice with viscous meal (50 g natto, 60 g Japanese yams and 40 g okras), and the control meal, comprising 200 g of white rice with non-viscous boiled soybeans, potatoes and broccoli, contained comparable amounts of carbohydrate, fat, protein and fiber. In addition, whiter rice was used as a reference meal. Blood samples over 180 min were analyzed for glucose, insulin, non-esterified free fatty acid and triacylglyceride. Peak glucose and insulin concentrations after the test meal (6.0 mmol/L and 262 pmol/L) were significantly lower than after the control meal (6.8 mmol/L and 360 pmol/L). The incremental areas under the curve for glucose and insulin over 0-120 min after the test meal were also significantly reduced as compared with the control meal (28 and 27%). The consumption of naturally viscous vegetables with white rice reduced acute glycemia and insulinemia. This practical dietary combination would ensure compliance and favorably alter the risk for diabetes and cardiovascular diseases. (Keyword) Adult / Area Under Curve / Blood Glucose / Cross-Over Studies / Diabetes Mellitus, Type 2 / Dietary Fiber / Female / fermentation / Glycemic Index / Humans / insulin / Japan / Lipids / Male / Oryza sativa / Patient Compliance / Postprandial Period / Soy Foods / Vegetables / Young Adult (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19114406 ● Summary page in Scopus @ Elsevier: 2-s2.0-63849158772 (PubMed: 19114406, Elsevier: Scopus)
67.	J. Sekizawa, Y. Kojima, K. Mihara, Hironori Yamamoto, N. Ohta, A. Harada, Eiji Takeda, N. Yamada, T. Ikeuchi, Y. Imamura, Y. Nakamura and S. Miyairi : Urine concentrations of indirubin in rats and humans and its possible interaction with other aryl hydrocarbon receptor ligands, Presistent organic pollutants(pops)research in asia, 2008.
68.	Takashi Uebanso, Hidekazu Arai, Yutaka Taketani, Makiko Fukaya, Hironori Yamamoto, Akira Mizuno, Keisuke Uryu, Takahiko Hada and Eiji Takeda : Extracts of Momordica charantia suppress postprandial hyperglycemia in rats., Journal of Nutritional Science and Vitaminology, Vol.53, No.6, 482-488, 2007. (Summary) Momordica charantia (bitter melon) is commonly known as vegetable insulin, but the mechanisms underlying its hypoglycemic effect remain unclear. To address this issue, the effects of bitter melon extracts on postprandial glycemic responses have been investigated in rats. An aqueous extract (AE), methanol fraction (MF) and methanol insoluble fraction (MIF) were prepared from bitter melon. An oral sucrose tolerance test revealed that administration of AE, MF or MIF each significantly suppressed plasma glucose levels at 30 min as compared with the control. In addition, the plasma insulin level at 30 min was also significantly lower after MF administration than in the control in the oral sucrose tolerance test. By contrast, these effects of bitter melon extracts were not observed in the oral glucose tolerance test. In terms of mechanism, bitter melon extracts dose-dependently inhibited the sucrase activity of intestinal mucosa with IC(50) values of 8.3, 3.7 and 12.0 mg/mL for AE, MF and MIF, respectively. The fraction with a molecular weight of less than 1,300 (LT 1,300) obtained from MF inhibited the sucrase activity most strongly in an uncompetitive manner with an IC(50) value of 2.6 mg/mL. Taken together, these results demonstrated that bitter melon suppressed postprandial hyperglycemia by inhibition of alpha-glucosidase activity and that the most beneficial component is present in the LT 1,300 fraction obtained from MF. (Keyword) Animals / Blood Glucose / Enzyme Inhibitors / Hyperglycemia / Insulin / Male / Momordica charantia / Plant Preparations / Postprandial Period / Rats / Rats, Sprague-Dawley / Sucrase / alpha-Glucosidases (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.53.482 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18202535 ● Search Scopus @ Elsevier (PMID): 18202535 ● Search Scopus @ Elsevier (DOI): 10.3177/jnsv.53.482 (DOI: 10.3177/jnsv.53.482, PubMed: 18202535)
69.	Yutaka Taketani, Emi Shuto, Hidekazu Arai, Yuka Nishida, Rieko Tanaka, Takashi Uebanso, Hironori Yamamoto, Hisami Okumura and Eiji Takeda : Advantage of a low glycemic index and low phosphate diet on diabetic nephropathy and aging-related diseases., The Journal of Medical Investigation : JMI, Vol.54, No.3-4, 359-365, 2007. (Summary) Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD) in Japan and other Westernized countries. Over 50% of the ESRD patients die from cardiovascular events. Cardiovascular disease (CVD) in ESRD patients with diabetes mellitus (DM) are implicated in the endothelial dysfunction caused by hyperglycemia, hyperlipidemia, and hypertension, and in the vascular calcification of intimal and medial arterial blood vessels caused by hyperphosphatemia. Therefore, dietary control of hyperglycemia and hyperphosphatemia should play an important role in the management of ESRD patients with DM. Furthermore, recent findings suggest that high concentrations of serum phosphate, even if within the normal range, may be a risk factor for CVD and mortality. An in vivo study using klotho knockout mice and fibroblast growth factor 23 (FGF-23) knockout mice has revealed that correction of hyperphosphatemia and hypervitaminosis D could ameliorate the premature aging-like phenotype. A low glycemic index and low phosphate diet may provide an advantage in the prevention of aging-related diseases in healthy individuals as well as in those with chronic kidney disease. (Keyword) Aging / Animals / Diabetic Nephropathies / Glycemic Index / Humans / Kidney Failure, Chronic / Mice / Mice, Knockout / Phosphates / Phosphorus, Dietary (Tokushima University Institutional Repository) ● Metadata: 111542 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.54.359 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878688 ● Search Scopus @ Elsevier (PMID): 17878688 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.54.359 (Tokushima University Institutional Repository: 111542, DOI: 10.2152/jmi.54.359, PubMed: 17878688)
70.	Dai Matsumoto, Hisami Okumura, Hidekazu Arai, Masae Sakuma, Hironori Yamamoto, Yutaka Taketani, Yoshiko Tani, Yuji Morine, Mitsuo Shimada and Eiji Takeda : Nutritional treatment of a patient with hepatic cirrhosis with the novel low glycemic index liquid food (Inslow)., The Journal of Medical Investigation : JMI, Vol.54, No.3-4, 375-380, 2007. (Summary) A sixty-six year-old patient with liver cirrhosis and diabetes was nutritionally treated by administration of the low glycemic index liquid food (Inslow) as a late evening sack (LES) for 6 weeks. The mean energy intake increased from 825+/-48 kcal/d to 1567+/-66 kcal/d after the 6-week treatment period. The fasting glucose level did not change, remaining at about 100 mg/dl throughout this period. Interestingly, the amount of insulin administered was reduced from 38 units before treatment to 28 units in the fifth week of treatment without a change in the fasting glucose level. This indicates a marked improvement in insulin sensitivity due to Inslow administration in this patient. In conclusion, the long-term administration of Inslow as an LES may be an effective treatment for cirrhotic patients. (Keyword) Aged / Blood Glucose / Diabetes Complications / Energy Intake / Enteral Nutrition / Glycemic Index / Humans / Liver Cirrhosis / Male (Tokushima University Institutional Repository) ● Metadata: 111545 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.54.375 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878691 ● Search Scopus @ Elsevier (PMID): 17878691 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.54.375 (Tokushima University Institutional Repository: 111545, DOI: 10.2152/jmi.54.375, PubMed: 17878691)
71.	Kazusa Sato, Hidekazu Arai, Akira Mizuno, Makiko Fukaya, Tadatoshi Sato, Megumi Koganei, Hajime Sasaki, Hironori Yamamoto, Yutaka Taketani, Toshio Doi and Eiji Takeda : Dietary palatinose and oleic acid ameliorate disorders of glucose and lipid metabolism in zucker fatty rats., The Journal of Nutrition, Vol.137, No.8, 1908-1915, 2007. (Summary) Excessive dietary intake of carbohydrates and fats has been linked to the development of obesity. However, the mechanism by which these dietary factors interact to bring about metabolic changes has not been elucidated. We examined the combined effects of different types of dietary carbohydrates and fats on the etiology of obesity and its complications in the Zucker fatty (fa/fa) rat, a model of obesity. Specifically, these rats were fed an isocaloric diet containing various combinations of carbohydrates [palatinose (P), an insulin-sparing sucrose analogue, and sucrose (S)] and fatty acids [oleic acid (O) and linoleic acid (L)]. After 8 wk, palatinose feeding (PO and PL) led to significant reductions in visceral fat mass, adipocyte cell size, hyperglycemia, and hyperlipidemia compared with sucrose feeding (SO and SL); pancreatic islet hypertrophy was also prevented by palatinose feeding. Linoleic-acid-fed rats (PL and SL) exhibited reduced insulin-immunoreactive staining of the pancreatic islets, enhanced macrophage infiltration in adipose tissue, and an elevated plasma tumor necrosis factor-alpha concentration when compared with oleic-acid-fed rats (PO and SO). Furthermore, sucrose and linoleic acid synergistically increased the expression of genes involved in hepatic gluconeogenesis and lipogenesis [sterol regulatory-element binding protein (SREBP)-1c and SREBP-2]. In conclusion, a diet containing palatinose and oleic acid may prevent diet-induced metabolic abnormalities. The combination of palatinose and oleic acid holds promise for a new approach to preventing and treating obesity and its complications. (Keyword) Adipose Tissue / Animals / Blood Glucose / Body Weight / Diet / Gene Expression Regulation / Glucose / Inflammation / Isomaltose / Lipid Metabolism / Liver / Male / Oleic Acid / Pancreas / Rats / Rats, Zucker / Triglycerides (Link to Publication Site) ● Publication site (DOI): 10.1093/jn/137.8.1908 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17634263 ● CiNii @ National Institute of Informatics (CRID): 1574231876211155328 ● Search Scopus @ Elsevier (PMID): 17634263 ● Search Scopus @ Elsevier (DOI): 10.1093/jn/137.8.1908 (DOI: 10.1093/jn/137.8.1908, PubMed: 17634263, CiNii: 1574231876211155328)
72.	Naoki Sawada, Yutaka Taketani, Norio Amizuka, Masako Ichikawa, Chiharu Ogawa, Kaori Nomoto, Kunitaka Nashiki, Tadatoshi Sato, Hidekazu Arai, Masashi Isshiki, Hiroko Segawa, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : Caveolin-1 in extracellular matrix vesicles secreted from osteoblasts., Bone, Vol.41, No.1, 52-58, 2007. (Summary) Caveolin-1 is an essential and signature protein of caveolae, which are small invaginations of the plasma membrane enriched in cholesterol and sphingolipids. Although high levels of expression of caveolin-1 have been demonstrated in osteoblasts as well as endothelial cells, fibroblasts, and muscular cells, the role of caveolin-1 in osteoblasts has not been clarified. Here, we show that caveolin-1 is secreted from osteoblasts in the form of matrix vesicles; extracellular vesicles released from the plasma membrane of osteoblasts. In this study, caveolae and matrix vesicles were similarly enriched in cholesterol and sphingomyelin in fractions isolated from mineralizing MC3T3-E1 cells. Interestingly, in the MC3T3-E1 cells caveolin-1 was enriched in the matrix vesicle fraction as well as the caveolar membrane fraction, and the amount of caveolin-1 in the matrix vesicle fraction increased as differentiation progressed. Localization of caveolin-1 in matrix vesicles was also confirmed in murine tibia. Furthermore, overexpression of caveolin-1 enhanced matrix calcification in MC3T3-E1 cells, whereas knockdown of caveolin-1 diminished it. These results suggest that secreted caveolin-1 as a component of matrix vesicles may play an important role in osteoblast calcification. (Keyword) 3T3 Cells / Alkaline Phosphatase / Animals / Base Sequence / Calcification, Physiologic / Caveolin 1 / Cell Differentiation / Cholesterol / DNA Primers / Extracellular Matrix / Gene Expression / Mice / Microscopy, Immunoelectron / Osteoblasts / Phosphates / RNA Interference / Secretory Vesicles / Sphingomyelins / Tibia (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2007.02.030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17448744 ● Search Scopus @ Elsevier (PMID): 17448744 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2007.02.030 (DOI: 10.1016/j.bone.2007.02.030, PubMed: 17448744)
73.	Akira Mizuno, Hidekazu Arai, Makiko Fukaya, Mitsuyo Sato, Hisami Okumura, Eiji Takeda and Toshio Doi : Early-phase insulin secretion is distributed in obese subjects with glucose intolerance., Metabolism: Clinical and Experimental, Vol.56, No.6, 856-862, 2007. (Summary) The loss of early-phase insulin secretion is a characteristic feature of type 2 diabetes mellitus. The aim of this study is to examine when impairment of early-phase insulin secretion occurs and whether it can be related to increase in insulin resistance caused by obesity. We developed an analytical method to qualify the early-phase insulin secretion; that is, we measured C-peptide immunoreactivity (CPR) response to a selective increase in blood glucose level in portal vein during oral glucose load under a euglycemic hyperinsulinemic clamp (clamp-OGL). Glucose infusion rate, hepatic glucose uptake, and CPR response during clamp-OGL were measured in 30 subjects with diabetes who were divided into 3 groups based on body mass index, 13 obese subjects with normal glucose tolerance (O-NGT), 10 obese subjects with impaired glucose tolerance (O-IGT), and 15 healthy subjects. Significant increase in CPR levels at 10 minutes in clamp-OGL compared with those at steady state was observed in healthy subjects and in O-NGT; however, those were small or absent in diabetic patients and in O-IGT. The incremental ratio of CPR was not correlated to the makers of insulin resistance. The early-phase insulin secretion is well maintained in O-NGT; however, early-phase insulin secretion has already been disturbed in obese subjects with glucose intolerance. (Keyword) Adult / Aged / Blood Glucose / C-Peptide / Female / Glucose Intolerance / Glucose Tolerance Test / Humans / Insulin / Male / Middle Aged / Obesity (Link to Publication Site) ● Publication site (DOI): 10.1016/j.metabol.2007.01.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17512320 ● Search Scopus @ Elsevier (PMID): 17512320 ● Search Scopus @ Elsevier (DOI): 10.1016/j.metabol.2007.01.017 (DOI: 10.1016/j.metabol.2007.01.017, PubMed: 17512320)
74.	Makiko Fukaya, Akira Mizuno, Hidekazu Arai, Kazusa Muto, Takashi Uebanso, Kaoru Matuo, Hironori Yamamoto, Yutaka Taketani, Toshio Doi and Eiji Takeda : Mechanism of rapid-phase insulin response to elevation of portal glucose concentration., American Journal of Physiology, Endocrinology and Metabolism, Vol.293, No.2, E515-22, 2007. (Summary) The hepatoportal region is important for glucose sensing; however, the relationship between the hepatoportal glucose-sensing system and the postprandial rapid phase of the insulin response has been unclear. We examined whether a rapid-phase insulin response to low amounts of intraportal glucose infusion would occur, compared that with the response to intrajugular glucose infusion in conscious rats, and assessed whether this sensing system was associated with autonomic nerve activity. The increases in plasma glucose concentration did not differ between the two infusions at 3 min, but the rapid-phase insulin response was detected only in the intraportal infusion. A sharp and rapid insulin response was observed at 3 min after intraportal infusion of a small amount of glucose but not after intrajugular infusion. Furthermore, this insulin response was also induced by intraportal fructose infusion but not by nonmetabolizable sugars. The rapid-phase insulin response at 3 min during intraportal infusion did not differ between rats that had undergone hepatic vagotomy or chemical sympathectomy with 6-hydroxydopamine compared with control rats, but this response disappeared in rats that had undergone chemical vagotomy with atropine. We conclude that the elevation of glucose concentration in the hepatoportal region induced afferent signals from undetectable sensors and that these signals stimulate pancreas to induce the rapid-phase insulin response via cholinergic nerve action. (Keyword) Animals / Blood Glucose / Fructose / Glucose / Infusions, Intravenous / Insulin / Jugular Veins / Male / Mannose / Portal Vein / Rats / Rats, Sprague-Dawley / Sympathectomy, Chemical / Time Factors / Vagotomy (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00536.2006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17473051 ● Search Scopus @ Elsevier (PMID): 17473051 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00536.2006 (DOI: 10.1152/ajpendo.00536.2006, PubMed: 17473051)
75.	Yoshiko Tani, Tadashi Sato, Hisami Okumura, Hironori Yamamoto, Hidekazu Arai, Naoki Sawada, Kaori Genjida, Yutaka Taketani and Eiji Takeda : Effects of prolonged high phosphorus diet on phosphorus and calcium balance in rats., Journal of Clinical Biochemistry and Nutrition, Vol.40, No.3, 221-228, 2007. (Summary) The amount of phosphorus contained in food as food additives is currently increasing and a high intake of phosphorus can cause various diseases. To determine the effects of a prolonged high phosphorus diet, here we investigated the phosphorus and calcium balance and expression of type IIa sodium-dependent phosphate transporter (Npt IIa) in mature rats. Wistar male rats (8-weeks old) were divided into five groups and fed diets containing 0.6% calcium plus 0.3, 0.6, 0.9, 1.2 or 1.5% phosphorus for 4 weeks. Urinary and fecal phosphorus excretions were significantly increased by the high phosphorus diets (from 0.6 to 1.5%), dependent on the amount of dietary phosphorus. The net absorption of intestinal phosphorus was also significantly increased by high phosphorus diets. As a result, a negative phosphorus balance was observed in rats given the 1.2% or 1.5% phosphorus diets. Serum parathyroid hormone and 1,25-dihydroxyvitamin D(3) concentrations were increased by high phosphorus diets. In addition, high phosphorus diets decreased the expression of Npt IIa mRNA and protein in the renal brush border membrane. Taken together, these results suggest that diets containing 1.2 or 1.5% phosphorus plus 0.6% calcium have potentially adverse effects on phosphorus homeostasis in mature rat. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.40.221 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18398500 ● Search Scopus @ Elsevier (PMID): 18398500 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.40.221 (DOI: 10.3164/jcbn.40.221, PubMed: 18398500)
76.	Kaoru Matsuo, Hidekazu Arai, Kazusa Muto, Makiko Fukaya, Tadashi Sato, Akira Mizuno, Masae Sakuma, Hisami Okumura, Hajime Sasaki, Hironori Yamamoto, Yutaka Taketani, Toshio Doi and Eiji Takeda : The anti-obesity effect of the palatinose-based formula Inslow is likely due to an increase in the hepatic PPAR-α and adipocyte PPAR-γ gene expressions., Journal of Clinical Biochemistry and Nutrition, Vol.40, No.3, 234-241, 2007. (Summary) Abdominal obesity is a principal risk factor in the development of metabolic syndrome. Previously, we showed that a palatinose-based liquid formula, Inslow/MHN-01, suppressed postprandial plasma glucose level and reduced visceral fat accumulation better than the standard formula (SF). To elucidate the mechanism of Inslow-mediated anti-obesity effect, expression levels of genes involved in the glucose and lipid metabolism were compared in Inslow- and SF-fed rats. Both fasting plasma insulin level and average islet sizes were reduced in the Inslow group. We also found less abdominal fat accumulation and reduced hepatic triacylglycerol content in the Inslow group. Expression of the beta-oxidation enzymes and uncoupling potein-2 (UCP-2) mRNAs in the liver of the Inslow group were higher than the SF group, which was due to a concomitant higher expression of the peroxisome proliferator-activated receptor (PPAR)-alpha mRNA in the former. Furthermore, expression of the UCP-2 and adiponectin mRNAs in the epididymal fat were higher in the Inslow group than the SF group, and were stimulated by a concomitant increase of the PPAR-gamma gene expression in the former. These results strongly suggested that the anti-obesity effect of Inslow was due to an increase in the hepatic PPAR-alpha and adipocyte PPAR-gamma gene expressions. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.40.234 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18398502 ● Search Scopus @ Elsevier (PMID): 18398502 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.40.234 (DOI: 10.3164/jcbn.40.234, PubMed: 18398502)
77.	Hidekazu Arai, Akira Mizuno, Masae Sakuma, Makiko Fukaya, Kaoru Matsuo, Kazusa Muto, Hajime Sasaki, Motoi Matsuura, Hisami Okumura, Hironori Yamamoto, Yutaka Taketani, Toshio Doi and Eiji Takeda : Effects of a palatinose-based liquid diet (Inslow) on glycemic control and the second-meal effect in healthy men., Metabolism: Clinical and Experimental, Vol.56, No.1, 115-121, 2007. (Summary) Postprandial hyperglycemia induces prolonged hyperinsulinemia, which is a risk factor for type 2 diabetes mellitus. Foods with a low glycemic index blunt the rapid rise in postprandial plasma glucose and insulin levels. We herein investigated the effects of a novel, palatinose-based liquid diet (Inslow, Meiji Dairy Products, Tokyo, Japan) on postprandial plasma glucose and insulin levels and on the rate of substrate oxidation in 7 healthy men. Furthermore, to examine the effects of Inslow on the second-meal effect, we quantified our subjects' postprandial plasma glucose, insulin, and free fatty acid levels for up to 7 hours after they ingested a breakfast containing Inslow or control formula, followed by a standard lunch 5 hours later. Our results showed that peak plasma glucose and insulin levels 30 minutes after Inslow loading were lower than after control formula loading. Postprandial fat oxidation rates in the Inslow group were higher than in the control formula group (P < .05). In the second-meal effect study, plasma glucose and insulin levels after lunch in the Inslow group were lower than in the control formula group (P < .01), although the peak levels in these groups were not different. The free fatty acid concentration in the Inslow group immediately before lunch was significantly lower than in the control formula group (P < .05). In conclusion, consumption of Inslow at breakfast appears to improve patient glycemic control by reducing their postprandial plasma glucose and insulin levels after lunch (second-meal effect). (Keyword) Adult / Blood Glucose / Cross-Over Studies / Energy Metabolism / Fatty Acids, Nonesterified / Humans / Insulin / Isomaltose / Male / Oxidation-Reduction / Postprandial Period (Link to Publication Site) ● Publication site (DOI): 10.1016/j.metabol.2006.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17161233 ● Search Scopus @ Elsevier (PMID): 17161233 ● Search Scopus @ Elsevier (DOI): 10.1016/j.metabol.2006.09.005 (DOI: 10.1016/j.metabol.2006.09.005, PubMed: 17161233)
78.	Yoko Mizuha, Hironori Yamamoto, Tadatoshi Sato, Mitsuyoshi Tsuji, Masashi Masuda, Masayuki Uchida, Kentaro Sakai, Yutaka Taketani, Koji Yasutomo, Hajime Sasaki and Eiji Takeda : Water extract of Cordyceps sinensis (WECS) inhibits the RANKL-induced osteoclast differentiation., BioFactors, Vol.30, No.2, 105-116, 2007. (Summary) It has been reported that Cordyceps sinensis, a traditional Chinese medicine, has various pharmacological effects. The aim of this study was to clarify the effect of water extract of Cordyceps sinensis (WECS) on osteoclast differentiation in vitro. In mouse bone marrow cells and monocyte/macrophage cell line RAW264.7, WECS dose-dependently inhibited the receptor activator of nuclear factor kappa B (NF-kappaB) ligand (RANKL)-induced osteoclast differentiation by tartrate-resistant acid phosphatase (TRAP) staining. In fact, cytotoxic effect was not observed in the RAW264.7 cells treated with WECS. Moreover, the mRNA expression of osteoclast related genes (calcitonin receptor, cathepsin K, matrix metalloprotease 9 and nuclear factor of activated T cells c1) was also inhibited by WECS. Investigation of inhibitory mechanism by using electrophoretic mobility shift assay (EMSA) and Western blot analysis revealed that WECS inhibited the activation of NF-kappaB through the prevention of IkappaBalpha phosphorylation. In conclusion, the present results demonstrate for the first time that WECS is a potent inhibitor of the RANKL-induced osteoclast differentiation through a mechanism involving the NF-kappaB pathway. (Keyword) Animals / Bone Marrow Cells / Cathepsins / Cell Differentiation / Cells, Cultured / Cordyceps / Gene Expression / Macrophages / Male / Matrix Metalloproteinase 9 / Mice / Mice, Inbred C57BL / Monocytes / NF-kappa B / NFATC Transcription Factors / Osteoclasts / RANK Ligand / Receptors, Calcitonin (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18356582 ● Search Scopus @ Elsevier (PMID): 18356582 (PubMed: 18356582)
79.	Yuka Nishida, Yutaka Taketani, Hisami Okumura, Fumiaki Imamura, Akiko Taniguchi, Tadatoshi Sato, Emi Shuto, Kunitaka Nashiki, Hidekazu Arai, Hironori Yamamoto and Eiji Takeda : Acute effect of oral phosphate loading on serum fibroblast growth factor 23 levels in healthy men., Kidney International, Vol.70, No.12, 2141-2147, 2006. (Summary) Serum fibroblast growth factor 23 (FGF23) is a novel phosphaturic factor and important for the regulation of inorganic phosphate (Pi) homeostasis. In this study, we examined an acute effect of oral Pi loading on serum FGF23 levels to clarify the role in rapid adjustment of serum Pi level. We performed a randomized, double-blind, crossover study in eight healthy male volunteers. The subjects were alternately served one of three test meals containing different Pi amounts (400 mg (P400), 800 mg (P800), and 1200 mg (P1200)) as lunch at noon. The postprandial changes in serum levels of Pi, Ca, 1,25-dihydroxyvitamin D, intact-parathyroid hormone (iPTH), intact-FGF23 (iFGF23), and urinary excretion of Pi and Ca until 8 h after Pi loading were estimated. Serum Pi levels and urinary Pi excretion significantly increased within 1 h after P400 and P800 intake. Serum iPTH levels at 1-2 and 4-6 h after P1200 intake was significantly higher than those of P400 intake. Serum iFGF23 levels slightly decreased up to 8 h after P400 intake and up to 6 h after P800 intake, but not changed in P1200 intake. Significant increase of iFGF23 was observed at 8 h after P1200 intake compared with both P400 and P800 intake. Additionally, negative association was detected between iFGF23 and serum Pi, whereas positive association was observed between iPTH and serum Pi during the short period. We conclude that oral Pi loading cannot rapidly increase serum FGF23 level. FGF23 may be not associated with rapid adaptation of Pi homeostasis. (Keyword) Administration, Oral / Adult / calcium / Cross-Over Studies / Fibroblast Growth Factors / homeostasis / Humans / Male / Parathyroid Hormone / Phosphates / Vitamin D (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.ki.5002000 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17063170 ● Search Scopus @ Elsevier (PMID): 17063170 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.ki.5002000 (DOI: 10.1038/sj.ki.5002000, PubMed: 17063170)
80.	Tadatoshi Sato, Hironori Yamamoto, Naoki Sawada, Kunitaka Nashiki, Mitsuyoshi Tsuji, Kazusa Muto, H Kume, Hajime Sasaki, Hidekazu Arai, Takeshi Nikawa, Yutaka Taketani and Eiji Takeda : Restraint stress alters the duodenal expression of genes important for lipid metabolism in rat., Toxicology, Vol.227, No.3, 248-261, 2006. (Summary) Stress, such as trauma and injury, is known to cause transcriptional changes in various tissues; however, there is little information on tissue-specific gene expression in response to stress. Here, we have examined duodenal gene expression in rats subjected to whole-body immobilization in order to elucidate the mechanism underlying the stress response in the duodenum--one of the tissues that is most sensitive to external stress. DNA microarray analysis revealed that the immobilization for 2 weeks caused great changes in gene expression in the rat duodenum: 165 genes exhibited more than a two-fold change in expression level (103 up-regulated; 62 down-regulated). In addition, functional classification of these genes showed that immobilization preferentially stimulated the expression of genes related to lipid metabolism, including genes encoding mitochondrial HMG-CoA synthase, a key enzyme in ketogenesis; solute carrier 27A2, a fatty acid transporter; and dienoyl CoA reductase, a key enzyme in beta-oxidation. To elucidate the factors mediating these immobilization-induced changes, we treated rats and small intestinal IEC-6 cells with dexamethasone and hydrogen peroxide. In both rats and IEC-6 cells, treatment with dexamethasone induced changes in gene expression that mimicked the immobilization-mediated increase in expression of the mitochondrial HMG-CoA synthase and dienoyl CoA reductase transcripts, suggesting that stress-induced synthesis of glucocorticoid hormones mediates, at least in part, the stress response in the duodenum. These results suggest that immobilization may alter lipid metabolism in the small intestine by modifying the expression of specific genes through which the small intestine may seek to protect itself from stress-induced damage. (Keyword) Animals / Cell Line / Dexamethasone / Down-Regulation / Duodenum / Gene Expression / Hydrogen Peroxide / Lipid Metabolism / Male / Mitochondria / Oligonucleotide Array Sequence Analysis / Rats / Rats, Wistar / Restraint, Physical / Reverse Transcriptase Polymerase Chain Reaction / Stress, Psychological / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.tox.2006.08.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16962226 ● Search Scopus @ Elsevier (PMID): 16962226 ● Search Scopus @ Elsevier (DOI): 10.1016/j.tox.2006.08.009 (DOI: 10.1016/j.tox.2006.08.009, PubMed: 16962226)
81.	Hisami Okumura, Taki Nakamura, Harumi Takeuchi, Hidenori Miyake, Takafumi Katayama, Hidekazu Arai, Yutaka Taketani, Masahiko Fujii, Mitsuo Shimada and Eiji Takeda : Effect of late evening snack with rice ball on energy metabolism in liver cirrhosis., European Journal of Clinical Nutrition, Vol.60, No.9, 1067-1072, 2006. (Summary) This study investigates the effects of a late evening snack (LES), of 200 kcal of rice ball, on energy metabolism in cirrhotic patients. Impaired nutritional metabolism has been associated with cirrhosis, and frequent intake of small meals may prevent early-onset starvation, and maintain nourishment in these patients. Twenty-one cirrhotic patients and 26 control subjects (Control) were recruited for this study. Patients were subsequently treated by LES (LC-LES) and by a non-LES regimen (LC-NLES). Resting energy expenditure and respiratory quotient (RQ) were assessed by indirect calorimetry at 0830, 1130 and 1430. Blood glucose and non-esterified fatty acids (NEFA) were measured just before the energy metabolism measurements. The regular diet included three major meals and LES, at 0900, 1200, 1800 and 2100, respectively. The Control and LC-NLES groups received only the major meals, whereas the LC-LES group received three meals plus 200 kcal LES for 7 days. There was no difference in the total energy intake among Control, LC-NLES and LC-LES groups. Respiratory quotient in LC-NLES was significantly lower than that of Control at 0830. Respiratory quotient value in LC-LES significantly elevated from that in LC-NLES. The RQ values did not differ among Control, LC-NLES and LC-LES at 2 h after the meal (1130 and 1430). Non-esterified fatty acids in LC-LES were lower than that in LC-NLES after overnight fasting. The ingestion of a 200 kcal rice ball LES can improve the nutritional metabolism in cirrhotic patients. (Keyword) Basal Metabolism / Blood Glucose / Calorimetry, Indirect / Circadian Rhythm / Dietary Carbohydrates / Energy Metabolism / Fatty Acids, Nonesterified / Humans / Liver Cirrhosis / Male / Middle Aged / Oryza sativa / Oxygen Consumption (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.ejcn.1602420 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16508643 ● Search Scopus @ Elsevier (PMID): 16508643 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.ejcn.1602420 (DOI: 10.1038/sj.ejcn.1602420, PubMed: 16508643)
82.	Tadatoshi Sato, Hironori Yamamoto, Naoki Sawada, Kunitaka Nashiki, Mitsuyoshi Tsuji, Takeshi Nikawa, Hidekazu Arai, Kyoko Morita, Yutaka Taketani and Eiji Takeda : Immobilization decreases duodenal calcium absorption through a 1,25-dihydroxyvitamin D-dependent pathway., Journal of Bone and Mineral Metabolism, Vol.24, No.4, 291-299, 2006. (Summary) Immobilization induces significant and progressive bone loss, with an increase in urinary excretion and a decrease in intestinal absorption of calcium. These actions lead to negative calcium balance and the development of disuse osteoporosis. The aims of this study were to evaluate the molecular mechanisms of decreased intestinal calcium absorption and to determine the effect of dietary 1,25-dihydroxyvitamin D [1,25(OH)2D] and a high-calcium diet on bone loss due to immobilization. The immobilized rat model was developed in the Bollman cage III to induce systemic disuse osteoporosis in the animals. There was a significant decrease in lumbar bone mineral density (BMD) and intestinal calcium absorption in the immobilized group compared with the controls. Serum 25-hydroxyvitamin D concentration did not change, but 1,25(OH)2D concentration decreased significantly. The mRNA levels of renal 25-hydoxyvitamin D 24-hydroxylase (24OHase) increased, whereas those of renal 25-hydroxyvitamin D 1-alpha hydroxylase (1alpha-hydroxylase), duodenal transient receptor potential cation channel, subfamily V, member 6 (TRPV6), TRPV5, and calbindin-D9k were all decreased. A high-calcium diet did not prevent the reduction in lumbar BMD or affect the mRNA expression of proteins related to calcium transport. Dietary administration of 1,25(OH)2D increased the intestinal calcium absorption that had been downregulated by immobilization. TRPV6, TRPV5, and calbindin-D9k mRNA levels were also upregulated, resulting in prevention of the reduction in lumbar BMD. Therefore, it is concluded that dietary 1,25(OH)2D prevented decreases in intestinal calcium absorption and simultaneously prevented bone loss in immobilized rats. However, it remains unclear that calcium absorption and expression of calcium transport proteins are essential for the regulation of lumbar BMD. (Keyword) Animals / Calcium / Calcium, Dietary / Dihydroxycholecalciferols / Duodenum / Humans / Immobilization / Intestinal Absorption / Rats / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-006-0686-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16816923 ● Search Scopus @ Elsevier (PMID): 16816923 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-006-0686-z (DOI: 10.1007/s00774-006-0686-z, PubMed: 16816923)
83.	Eiji Takeda, Yutaka Taketani, Kunitaka Nashiki, Mayumi Nomoto, Emi Shuto, Naoki Sawada, Hironori Yamamoto and Masashi Isshiki : A novel function of phosphate-mediated intracellular signal transduction pathways, Advances in Enzyme Regulation, Vol.46, No.1, 154-161, 2006. (Keyword) Animals / Calcium Signaling / Cell Line / Endothelial Cells / Kidney Tubules, Proximal / Phosphates / reactive oxygen species / signal transduction / Swine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.advenzreg.2006.01.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16846635 ● Search Scopus @ Elsevier (PMID): 16846635 ● Search Scopus @ Elsevier (DOI): 10.1016/j.advenzreg.2006.01.003 (DOI: 10.1016/j.advenzreg.2006.01.003, PubMed: 16846635)
84.	Akihiko Kawaura, Eiji Takeda, Noritoshi Tanida, Kimie Nakagawa, Hironori Yamamoto, Kenji Sawada and Toshio Okano : Inhibitory Effect of Long Term 1α-Hydroxyvitamin D₃ Administration on Helicobacter pylori Infection, Journal of Clinical Biochemistry and Nutrition, Vol.38, No.2, 103-106, 2006. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.38.103 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-33645754907 (DOI: 10.3164/jcbn.38.103, Elsevier: Scopus)
85.	Hisami Okumura, 竹内晴美, 中村多希, Masahiko Fujii, Hidenori Miyake, Mitsuo Shimada and Eiji Takeda : 肝硬変患者における就寝前夜食療法継続指導の健康関連QOLに対する効果, 日本病態栄養学会誌, Vol.9, No.2, 159-164, 2006. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1574231875812577408 (CiNii: 1574231875812577408)
86.	Hironori Yamamoto, Yoshiko Tani, Kumi Kobayashi, Yutaka Taketani, Tadatoshi Sato, Hidekazu Arai, Kyoko Morita, Ken-ichi Miyamoto, John Wesley Pike, Shigeaki Kato and Eiji Takeda : Alternative promoters and renal cell-specific regulation of the mouse type IIa sodium-dependent phosphate cotransporter gene, Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1732, No.1-3, 43-52, 2005. (Summary) The type IIa sodium-dependent phosphate cotransporter (NPT2a) expressed in renal proximal tubules represents an important determinant in maintaining inorganic phosphate (Pi) homeostasis. In the present study, we identified two variant transcripts of the mouse NPT2a gene, Npt2a-v1 and Npt2a-v2, characterized by the presence of alternative first exons (either exon 1A or exon 1B). The chromosomal structure analysis revealed that the Npt2a gene comprises of two promoters (promoters 1 and 2) and 14 exons, and spans approximately 17 kb. Quantitative PCR analysis showed that renal mRNA levels of both the variants markedly decreased in X-linked vitamin D-resistant hypophosphatemic rickets (Hyp) mice compared to normal littermates. Interestingly, transcriptional activity of a reporter gene, containing Npt2a promoters 1 and 2, was renal cell-specifically increased by 1alpha, 25(OH)2D3 and its analogs. The deletion analysis revealed that the CAAT box in the Npt2a promoter 2 is important for the 1alpha, 25(OH)2D3-dependent renal cell-specific activation of the reporter gene. These data suggested that two alternative promoters control the renal expression of Npt2a gene and both Npt2a variant transcripts are down regulated in Hyp mice. (Keyword) 5' Flanking Region / 5' Untranslated Regions / Animals / Base Sequence / COS Cells / Caco-2 Cells / Calcitriol / Cells, Cultured / Cercopithecus aethiops / Chromosomes, Mammalian / Exons / Gene Expression Regulation / Humans / Kidney / Mice / Mice, Inbred C57BL / Mice, Obese / Molecular Sequence Data / Opossums / Organ Specificity / Promoter Regions, Genetic / RNA, Messenger / Sequence Deletion / Sodium-Phosphate Cotransporter Proteins, Type IIa (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbaexp.2005.11.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16380173 ● Search Scopus @ Elsevier (PMID): 16380173 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbaexp.2005.11.003 (DOI: 10.1016/j.bbaexp.2005.11.003, PubMed: 16380173)
87.	Kunitaka Nashiki, Yutaka Taketani, Tomoko Takeichi, Naoki Sawada, Hironori Yamamoto, Masako Ichikawa, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Role of membrane microdomains in PTH-mediated down-regulation of NaPi-IIa in opossum kidney cells, Kidney International, Vol.68, No.3, 1137-1147, 2005. (Summary) Parathyroid hormone (PTH) rapidly down-regulates type IIa sodium-dependent phosphate transporter (NaPi-IIa) via an endocytic pathway. Since the relationship between PTH signaling and NaPi-IIa endocytosis has not been explored, we investigated the role of membrane microdomains in this process. We examined the submembrane localization of NaPi-IIa in opossum kidney (OK-N2) cells that stably expressed human NaPi-IIa, and searched for a PTH-induced specific phosphorylating substrate on their membrane microdomains by immunoblotting with specific antibody against phospho substrates of protein kinases. We found that NaPi-IIa was primarily localized in low-density membrane (LDM) domains of the plasma membrane; PTH reduced the levels of immunoreactive NaPi-IIa in these domains. Furthermore, PTH activated both protein kinase A (PKA) and protein kinase Calpha (PKCa) and increased the phosphorylation of 250 kD and 80 kD substrates; this latter substrate was identified as ezrin, which a member of the ezrin-radixin-moesin (ERM) protein family. In response to PTH, ezrin was phosphorylated by both PKA and PKC. Dominant negative ezrin blocked the reduction in NaPi-IIa expression in the LDM domains that was induced by PTH. These data suggest that NaPi-IIa and PTH-induced phosphorylated proteins that include ezrin are compartmentalized in LDM microdomains. This compartmentalization may play an important role in the down-regulation of NaPi-IIa via endocytosis. (Keyword) Animals / Antineoplastic Agents / Cell Compartmentation / Cell Line / Chlorpromazine / Cyclic AMP-Dependent Protein Kinases / Cyclodextrins / Cytochalasin D / Cytoskeletal Proteins / Dopamine Antagonists / Down-Regulation / Endocytosis / Humans / Immunohistochemistry / Kidney / Nocodazole / Nucleic Acid Synthesis Inhibitors / Opossums / Parathyroid Hormone / Phosphates / Phosphoproteins / Phosphorylation / Protein Kinase C-alpha / Protein Structure, Tertiary / Sodium-Phosphate Cotransporter Proteins, Type IIa (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1523-1755.2005.00505.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16105044 ● Search Scopus @ Elsevier (PMID): 16105044 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1523-1755.2005.00505.x (DOI: 10.1111/j.1523-1755.2005.00505.x, PubMed: 16105044)
88.	竹内里美, 竹内晴美, Hisami Okumura, Hidekazu Arai, Yutaka Taketani, 山田静恵, 高橋保子 and Eiji Takeda : 血清アルブミン濃度からみたNST活動の意義と改善点, 日本病態栄養学会誌, Vol.8, No.1, 23-30, 2005.
89.	Junko Matsuda, Makiko Kido, Keiko Tadano-Aritomi, Ineo Ishizuka, Kumiko Tominaga, Kazunori Toida, Eiji Takeda, Kunihiko Suzuki and Yasuhiro Kuroda : Mutation in saposin D domain of sphingolipid activator protein gene causes urinary system defects and cerebellar Purkinje cell degeneration with accumulation of hydroxy fatty acid-containing ceramide in mouse, Human Molecular Genetics, Vol.13, No.21, 2709-2723, 2004. (Keyword) COLLISION-INDUCED DISSOCIATION / mass spectrometry / FARBERS DISEASE / DEFICIENT MICE / LEUKODYSTROPHY / PROSAPOSIN / DEATH / KIDNEY / MODEL / GLYCEROPLASMALOPSYCHOSINE (Link to Publication Site) ● Publication site (DOI): 10.1093/hmg/ddh281 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/hmg/ddh281 (DOI: 10.1093/hmg/ddh281)
90.	Eiji Takeda, 深谷牧子, 松尾薫 and Hidekazu Arai : 機能性食品と高齢者(消化器疾患)への臨床応用パラチノースの耐糖能障害への予防効果, 老年消化器病, Vol.16, No.2, 109-113, 2004. (Keyword) パラチノース / 食後高血糖 / 耐糖能障害予防
91.	Eiji Takeda, Junji Terao, Yutaka Nakaya, Ken-ichi Miyamoto, Yoshinobu Baba, Hiroshi Chuman, Ryuji Kaji, Tetsuro Ohmori and Kazuhito Rokutan : Stress control and human nutrition, The Journal of Medical Investigation : JMI, Vol.51, No.3-4, 139-145, 2004. (Summary) Stress is a pervasive factor in everyday life that critically affects development and functioning. Severe and prolonged stress exposure impairs homeostatic mechanisms, particularly associated with the onset of depressive illness. Brain food is aimed at preventing as well as treating a growing number of stress-related mental disorders. Some topics on the association of stress and nutrition is reviewed. (1) An increased activity of serotonergic neurons in the brain is an established consequence of stress. An increase in brain tryptophan levels on the order of that produced by eating a carbohydrate-rich/protein-poor meal causes parallel increases in the amounts of serotonin released into synapses. (2) Eating is thought to be suppressed during stress, due to anorectic effects of corticotrophin releasing hormone, and increased during recovery from stress, due to appetite stimulating effects of residual cortisol. (3) A strong inverse association between coffee intake and risk of suicide. (4) Night eating syndrome has been found to occur during periods of stress and is associated with poor results at attempts to lose weight and disturbances in the hypothalamic-pituitary-adrenal axis. (5) Dietary antioxidants present in fruits and vegetables may improve cognitive function. Therefore, it is concluded that the establishment of functional foods that correctly regulate stress response must be firmly based upon scientific knowledge and legal regulation. (Keyword) Antioxidants / brain / Coffee / Cognition / Dietary Carbohydrates / Feeding Behavior / Humans / Hydrocortisone / Nutritional Physiological Phenomena / Serotonin / Stress, Physiological / Suicide (Tokushima University Institutional Repository) ● Metadata: 110734 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.51.139 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15460899 ● Summary page in Scopus @ Elsevier: 2-s2.0-7044220587 (Tokushima University Institutional Repository: 110734, DOI: 10.2152/jmi.51.139, PubMed: 15460899, Elsevier: Scopus)
92.	Hidekazu Arai, Akira Mizuno, Kaoru Matsuo, Makiko Fukaya, Hajime Sasaki, Hirofumi Arima, Motoi Matsuura, Yutaka Taketani, Toshio Doi and Eiji Takeda : Effect of a novel palatinose-based liquid balanced formula (MHN-01) on glucose and lipid metabolism in male Sprague-Dawley rats after short- and long-term ingestion., Metabolism: Clinical and Experimental, Vol.53, No.8, 977-983, 2004. (Summary) Postprandial hyperglycemia and hyperinsulinemia are often present in obese subjects with glucose intolerance in whom insufficient early phase insulin secretion and subsequent delayed hyperinsulin response are observed. To address this problem, a novel palatinose-based enteral formula designated as MHN-01 was developed for the prevention of postprandial hyperglycemia and hyperinsulinemia. The effects of MHN-01 on carbohydrate and lipid metabolism in Sprague-Dawley (SD) rats were compared with those of the standard balanced formula (SBF). After a bolus intragastric injection of each formula equivalent to 0.9 g/kg carbohydrate, the peak levels of plasma glucose (PG) and insulin (IRI) in peripheral and portal veins of the MHN-01 group were significantly lower than those of the SBF group. The areas under the curve of PG and IRI in the MHN-01 group were 58.0% and 43.1% of those in the SBF group in the femoral vein and 65.0% and 69.3% in the portal vein, respectively. In the 2-month study, serum levels of IRI and triglyceride in peripheral blood in the MHN-01 group decreased and those in the SBF group increased compared with initial levels. Consequently, both levels in the MHN-01 group were significantly lower than those in the SBF group. In addition, the amount of accumulated fat in abdominal adipose tissue and liver tissue of the MHN-01 group was markedly reduced in comparison to that of the SBF group. Insulin sensitivity, evaluated as glucose infusion rate using the hyperinsulinemic euglycemic clamp technique, in the MHN-01 group was higher than that in the SBF group. Thus, in comparison to SBF, MHN-01 suppressed postprandial hyperglycemia and hyperinsulinemia, reduced visceral fat accumulation, and improved insulin sensitivity. Therefore, human study on the effects of MHN-01 on carbohydrate and lipid metabolism will be recommended to confirm whether MHN-01 may be a useful functional food for the treatment and prevention of insulin resistance. (Keyword) Algorithms / Animals / Blood Glucose / Body Weight / Catheterization / Dextrins / Diet / Dietary Fats / Eating / Enteral Nutrition / Food, Formulated / Glucose / Insulin / Insulin Resistance / Intubation, Gastrointestinal / Isomaltose / Lipids / Liver / Male / Organ Size / Parenteral Nutrition / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1016/j.metabol.2004.03.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15281004 ● Search Scopus @ Elsevier (PMID): 15281004 ● Search Scopus @ Elsevier (DOI): 10.1016/j.metabol.2004.03.004 (DOI: 10.1016/j.metabol.2004.03.004, PubMed: 15281004)
93.	関元幸代, 澄川一英 and Eiji Takeda : 健常者に対するカルシウム・イソフラボン含有錠を大量摂取した時の安全性の検討, 健康・栄養食品研究, Vol.7, No.1, 11-20, 2004. (Keyword) 錠菓 / 大豆イソフラボン / ビタミンD3 / 健常人 / chewable tablets / calcium / isoflavone / vitamin D3 / healthy volunteers / safety / large intake (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522543655945638912 (CiNii: 1522543655945638912)
94.	Eiji Takeda, Hironori Yamamoto, Kunitaka Nashiki, Tadatoshi Sato, Hidekazu Arai and Yutaka Taketani : Inorganic phosphate homeostasis and the role of dietary phosphorus., Journal of Cellular and Molecular Medicine, Vol.8, No.2, 191-200, 2004. (Summary) Inorganic phosphate (Pi) is required for cellular function and skeletal mineralization. Serum Pi level is maintained within a narrow range through a complex interplay between intestinal absorption, exchange with intracellular and bone storage pools, and renal tubular reabsorption. The crucial regulated step in Pi homeostasis is the transport of Pi across the renal proximal tubule. Type II sodium-dependent phosphate (Na/Pi) cotransporter (NPT2) is the major molecule in the renal proximal tubule and is regulated by Pi, parathyroid hormone and by 1,25-dihydroxyvitamin D. Recent studies of inherited and acquired hypophosphatemia [X-linked hypophosphatemic rickets/osteomalacia (XLH), autosomal dominant hypophosphatemic rickets/osteomalacia (ADHR) and tumor-induced rickets/osteomalacia (TIO)], which exhibit similar biochemical and clinical features, have led to the identification of novel genes, PHEX and FGF23, that play a role in the regulation of Pi homeostasis. The PHEX gene, which is mutated in XLH, encodes an endopeptidase, predominantly expressed in bone and teeth, but not in kidney. FGF-23 may be a substrate of this endopeptidase and may therefore accumulate in patients with XLH. In the case of ADHR mutations in the furin cleavage site, which prevent the processing of FGF-23 into fragments, lead to the accumulation of a "stable" circulating form of the peptide which also inhibits renal Pi reabsorption. In the case of TIO, ectopic overproduction of FGF-23 overwhelms its processing and degradation by PHEX, leading to the accumulation of FGF-23 in the circulation and inhibition of renal Pi reabsorption. Mice homozygous for severely hypomorphic alleles of the Klotho gene exhibit a syndrome resembling human aging, including atherosclerosis, osteoporosis, emphysema, and infertility. The KLOTHO locus is associated with human survival, defined as postnatal life expectancy, and longevity, defined as life expectancy after 75. In considering the relationship of klotho expression to the dietary Pi level, the klotho protein seemed to be negatively controlled by dietary Pi. (Keyword) Animals / Diet / Homeostasis / Humans / Hypophosphatemia, Familial / Osteomalacia / Phosphates (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1582-4934.2004.tb00274.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15256067 ● Summary page in Scopus @ Elsevier: 2-s2.0-16544393013 (DOI: 10.1111/j.1582-4934.2004.tb00274.x, PubMed: 15256067, Elsevier: Scopus)
95.	Naoya Ikeda, Hiroji Uemura, Hitoshi Ishiguro, Mayumi Hori, Masahiko Hosaka, Satoru Kyo, Ken-ichi Miyamoto, Eiji Takeda and Yoshinobu Kubota : Combination Treatment with 1α,25-Dihydroxyvitamin D₃ and 9-cis-Retinoic Acid Directly Inhibits Human Telomerase Reverse Transcriptase Transcription in Prostate Cancer Cells, Molecular Cancer Therapeutics, Vol.2, No.8, 739-746, 2003. (Summary) The vitamin D(3) receptor, which is the nuclear receptor for 1alpha,25-dihydroxyvitamin D(3) (VD(3)), forms a heterodimer with the retinoid X receptor (RXR), which is the nuclear receptor for 9-cis-retinoic acid (9-cis-RA). The heterodimer binds to a specific response element consisting of two directly repeated pairs of motifs, AGGTGA, spaced by three nucleotides [direct repeat (DR) 3] and modulates the expression of VD(3)-responsive genes. Telomerase activity, which is seen in most immortal cells and germ cells, is a complex of enzymes that maintain the length of telomeres. One of the major components of human telomerase, human telomerase reverse transcriptase (hTERT), is the catalytic subunit, and the expression of hTERT might correlate most strongly with telomerase activity. We found that the sequence of 5'-AGTTCATGGAGTTCA-3' (DR3') is similar to that of DR3 in the promoter region of hTERT. Our results showed that the combination of VD(3) and 9-cis-RA inhibited telomerase activity through direct interaction of the heterodimer of vitamin D(3) receptor and RXR with the DR3' sequence in the hTERT promoter as well as the combination of VD(3) and selective RXR ligand did. Also, in vivo data showed that the growth of xenografts in nude mice was inhibited by VD(3) and 9-cis-RA. The results of the present study provide evidence on the molecular mechanism of the inhibition of cell growth by these agents, and they could be novel therapeutic agents for prostate cancer. (Keyword) Animals / Antineoplastic Agents / Calcitriol / DNA-Binding Proteins / Drug Synergism / Humans / Male / Mice / Promoter Regions, Genetic / Prostatic Neoplasms / Reverse Transcriptase Polymerase Chain Reaction / Telomerase / Transcription, Genetic / Tretinoin / Tumor Cells, Cultured (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12939463 ● Search Scopus @ Elsevier (PMID): 12939463 (PubMed: 12939463)
96.	Tomoko Koda, Hisanori Minami, Tadashi Ogawa, Mariko Yamano and Eiji Takeda : Higher Concentrations of Interferon-γ Enhances Uptake and Transport of Dietary Antigens by Human Intestinal Cells: A Study Using Cultured Caco-2 Cells, Journal of Nutritional Science and Vitaminology, Vol.49, No.3, 179-186, 2003. (Summary) Besides functioning as a mucosal barrier and transporting nutrients, intestinal epithelial cells (IECs) also serve as antigen-presenting cells (APCs). Modification of protein antigens by proteolysis is one of the principal steps in antigen presentation to Th cells. We used a Caco-2 intestinal epithelial cell line to investigate the transepithelial transport of the dietary antigen, ovalbumin (OVA). We also examined the effects of the proinflammatory cytokine interferon-gamma (IFN-gamma) on the antigen transport process in Caco-2 cell layers. Caco-2 cell layers transferred both intact and degraded OVA from the mucosal to the serosal side. IFN-gamma stimulated OVA transport and most of the transported OVA in such cells were degraded. We also examined OVA uptake by Caco-2 cells using immunohistochemical means. Caco-2 cells incorporated OVA in a time-dependent manner and IFN-gamma significantly enhanced antigen internalization. Flow cytometry also demonstrated that IFN-gamma elevated the internalization of FITC-OVA. We also determined the effects of low and high concentrations of IFN-gamma on mucosal permeability and internalization of FITC-OVA. Although both 10 and 50 ng/mL IFN-gamma stimulated mucosal permeability to the same extent, more FITC-OVA was internalized by Caco-2 cells incubated with 50 than with 10 ng/mL IFN-gamma. These results suggest that the effects of IFN-gamma on mucosal permeability and the internalization of antigens by intestinal epithelial cells are brought about by different mechanisms. Therefore, higher concentrations of IFN-gamma stimulate the uptake, processing, and transport of dietary antigens by IECs. (Keyword) Caco-2 cells / ovalbumin (OVA) / transcellular transport / interferon (IFN)-γ / antigen uptake (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12953796 ● CiNii @ National Institute of Informatics (CRID): 1390001206324962176 ● Summary page in Scopus @ Elsevier: 2-s2.0-0042312394 (PubMed: 12953796, CiNii: 1390001206324962176, Elsevier: Scopus)
97.	Yutaka Taketani, Mayumi Nomoto, Hironori Yamamoto, Masashi Isshiki, Kyoko Morita, Hidekazu Arai, Ken-ichi Miyamoto, Shigeaki Kato and Eiji Takeda : Increase in IP3 and intracellular Ca²⁺ induced by phosphate depletion in LLC-PK₁ cells., Biochemical and Biophysical Research Communications, Vol.305, No.2, 287-291, 2003. (Summary) The mechanisms by which Pi depletion rapidly regulates gene expression and cellular function have not been clarified. Here, we found a rapid increase in intracellular ionized calcium [Ca(2+)](i) by phosphate depletion in LLC-PK(1) cells using confocal microscopy with the green-fluorescence protein based calcium indicator "yellow cameleon 2.1." The increase of [Ca(2+)](i) was observed in the presence or absence of extracellular Ca(2+). At the same time, an approximately twofold increase in intracellular inositol 1,4,5-triphosphate (IP(3)) occurred in response to the acute Pi depletion in the medium. Furthermore, 2-aminoethoxydiphenyl borate completely blocked the [Ca(2+)](i) increase induced by Pi depletion. These results suggest that Pi depletion causes IP(3)-mediated release of Ca(2+) from intracellular Ca(2+) pools and rapidly increases [Ca(2+)](i) in LLC-PK(1) cells. (Keyword) Animals / Boron Compounds / Calcium / Cell Line / Cytoplasm / Inositol 1,4,5-Trisphosphate / Kidney Tubules, Proximal / Kinetics / Microscopy, Confocal / Phosphates / Rats (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-291X(03)00750-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12745071 ● Search Scopus @ Elsevier (PMID): 12745071 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-291X(03)00750-2 (DOI: 10.1016/S0006-291X(03)00750-2, PubMed: 12745071)
98.	中村多希, Hisami Okumura, 津田紀子, Akira Mizuno, Hidenori Miyake, Seiki Tashiro, 鶴尾美穂 and Eiji Takeda : 肝硬変患者に対する就寝前夜食(LES)療法の長期継続効果:エネルギー代謝および耐糖能異常の改善がみられた1症例, 栄養-評価と治療, Vol.19, No.4, 461-465, 2002.
99.	芳田美智子, Hironori Yamamoto, Kyoko Morita and Eiji Takeda : スタニオカルシン2の分泌機構, Journal of Developmental Nephrology, Vol.10, No.1, 50-56, 2002.
100.	Eiji Takeda, Kyoko Sakamoto, Kimi Yokota, Maiko Shinohara, Yutaka Taketani, Kyoko Morita, Hironori Yamamoto, Ken-ichi Miyamoto and Mitsuo Shibayama : Phosphorus supply per capita from food in Japan between 1960 and 1995, Journal of Nutritional Science and Vitaminology, Vol.48, No.2, 102-108, 2002. (Summary) The awareness of phosphorus intake is important because hyperphosphatemia and hypophosphatemia both impair bone metabolism. Phosphorus consumption from food was obtained from values in the Food Balance Sheet (PBS) of Japan from 1960 to 1995. The amounts of phosphorus calculated from the FBS increased gradually from 1,243 mg/d in 1960 to 1,332 mg/d in 1975 and to 1,421 mg/d in 1995. This is explained by the increased consumption of cow's milk and milk products, meat, and chicken eggs. The main foods supplying phosphorus in 1995 were cereals, milk and milk products, fishes and shellfishes, and vegetables; their contributions were 24.4, 15.8, 14.2, and 10.9%, respectively. The phosphorus-to-calcium ratio calculated from the FBS was 3.51 in 1960, which decreased to 2.89 in 1975 and 2.44 in 1995. Therefore total phosphorus consumption in 1995 was presumably more than 1,500 mg/d when imported food containing phosphorus and the consumption of phosphorus-containing food additives in Japan are also considered. These findings suggest that the phosphorus consumption estimated from the FBS is increasing and that more attention should be paid to the maintenance of healthy bones in Japan, where the average amount of calcium intake is less than 600 mg/d. (Keyword) Bone and Bones / Calcium, Dietary / Food Analysis / Food Supply / Humans / Japan / Nutritional Requirements / phosphorus / Phosphorus, Dietary (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12171429 ● Search Scopus @ Elsevier (PMID): 12171429 (PubMed: 12171429)
101.	Yuki Suzaki, Masanori Yoshizumi, Shoji Kagami, Hajime Koyama, Yutaka Taketani, Hitoshi Houchi, Koichiro Tsuchiya, Eiji Takeda and Toshiaki Tamaki : Hydrogen Peroxide Stimulates c-Src-mediated Big Mitogen-activated Protein Kinase 1(BMK1) and the MEF2C Signaling Pathway in PC12 Cells, The Journal of Biological Chemistry, Vol.277, No.11, 9614-9621, 2002. (Summary) Reactive oxygen species, generated by reduction-oxidation (redox) reactions, have been recognized as one of the major mediators of ischemia and reperfusion injury in the brain. Reactive oxygen species-induced cerebral events are attributable, in part, to the change in intracellular signaling molecules including mitogen-activated protein (MAP) kinases. Big MAP kinase 1 (BMK1), also known as ERK5, is a newly identified member of the MAP kinase family and has been reported to be sensitive to oxidative stress. In the present study, we examined the effect of H(2)O(2) on BMK1 activity in PC12 cells, and we investigated the pathophysiological implication of BMK1. Findings showed that BMK1 was rapidly and significantly activated by H(2)O(2) in a concentration-dependent manner in PC12 cells. BMK1 activation by H(2)O(2) was inhibited by both PD98059 and U0126, which were reported to inhibit MEK5 as well as MEK1/2. c-Src was suggested to be involved in BMK1 activation from the experiments with herbimycin A and PP2, specific inhibitors of Src family kinases. Transfection of kinase-inactive Src also inhibited H(2)O(2)-induced BMK1 activation. In addition, H(2)O(2) treatment of cells induced an enhancement of DNA binding activity of MEF2C, a downstream transcription factor of BMK1 in PC12 cells. Finally, pretreatment of cells with PD98059 and U0126 resulted in an increase in cell death including apoptosis by H(2)O(2) in ERK1/2 down-regulated cells as well as in intact PC12 cells. These findings suggest that c-Src mediated BMK1 activation by H(2)O(2) may counteract ischemic cellular damage probably through the activation of MEF2C transcription factor. (Keyword) CENTRAL-NERVOUS-SYSTEM / SMOOTH-MUSCLE CELLS / PROTEIN-KINASE-1 BMK1 / TRANSDUCTION PATHWAY / NEURONAL DIFFERENTIATION / CEREBRAL-ISCHEMIA / TYROSINE KINASES / OXYGEN RADICALS / GENE-EXPRESSION / JUN PROMOTER (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M111790200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11782488 ● CiNii @ National Institute of Informatics (CRID): 1573950401500650880 ● Search Scopus @ Elsevier (PMID): 11782488 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111790200 (DOI: 10.1074/jbc.M111790200, PubMed: 11782488, CiNii: 1573950401500650880)
102.	Osamu Yanagida, Yoshikatsu Kanai, Arthit Chairoungdua, Do Kyung Kim, Hiroko Segawa, Tomoko Nii, Seok Ho Cha, Hirotaka Matsuo, Jun-ichi Fukushima, Yoshiki Fukasawa, Yoshiko Tani, Yutaka Taketani, Hiroshi Uchino, Ju Young Kim, Jun Inatomi, Isao Okayasu, Ken-ichi Miyamoto, Eiji Takeda, Tomoyuki Goya and Hitoshi Endou : Human L-type amino acid transporter 1(LAT1):/characterization of function and expression in tumor cell lines, Biochimica et Biophysica Acta (BBA) - Biomembranes, Vol.1514, No.2, 291-302, 2001. (Summary) System L is a major nutrient transport system responsible for the transport of large neutral amino acids including several essential amino acids. We previously identified a transporter (L-type amino acid transporter 1: LAT1) subserving system L in C6 rat glioma cells and demonstrated that LAT1 requires 4F2 heavy chain (4F2hc) for its functional expression. Since its oncofetal expression was suggested in the rat liver, it has been proposed that LAT1 plays a critical role in cell growth and proliferation. In the present study, we have examined the function of human LAT1 (hLAT1) and its expression in human tissues and tumor cell lines. When expressed in Xenopus oocytes with human 4F2hc (h4F2hc), hLAT1 transports large neutral amino acids with high affinity (K(m)= approximately 15- approximately 50 microM) and L-glutamine and L-asparagine with low affinity (K(m)= approximately 1.5- approximately 2 mM). hLAT1 also transports D-amino acids such as D-leucine and D-phenylalanine. In addition, we show that hLAT1 accepts an amino acid-related anti-cancer agent melphalan. When loaded intracellularly, L-leucine and L-glutamine but not L-alanine are effluxed by extracellular substrates, confirming that hLAT1 mediates an amino acid exchange. hLAT1 mRNA is highly expressed in the human fetal liver, bone marrow, placenta, testis and brain. We have found that, while all the tumor cell lines examined express hLAT1 messages, the expression of h4F2hc is varied particularly in leukemia cell lines. In Western blot analysis, hLAT1 and h4F2hc have been confirmed to be linked to each other via a disulfide bond in T24 human bladder carcinoma cells. Finally, in in vitro translation, we show that hLAT1 is not a glycosylated protein even though an N-glycosylation site has been predicted in its extracellular loop, consistent with the property of the classical 4F2 light chain. The properties of the hLAT1/h4F2hc complex would support the roles of this transporter in providing cells with essential amino acids for cell growth and cellular responses, and in distributing amino acid-related compounds. (Keyword) Amino Acid Transport Systems / Amino Acids, Essential / Animals / Antigens, CD / Antigens, CD98 / Carrier Proteins / DNA Probes / DNA, Complementary / Fetus / Humans / Molecular Sequence Data / Oocytes / Protein Biosynthesis / RNA, Complementary / RNA, Messenger / Substrate Specificity / Tumor Cells, Cultured / Xenopus (Link to Publication Site) ● Publication site (DOI): 10.1016/S0005-2736(01)00384-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11557028 ● Search Scopus @ Elsevier (PMID): 11557028 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2736(01)00384-4 (DOI: 10.1016/S0005-2736(01)00384-4, PubMed: 11557028)
103.	Tomoko Nii, Hiroko Segawa, Yutaka Taketani, Yoshiko Tani, Makiko Ohkido, Sachie Kishida, Mikiko Ito, Hitoshi Endou, Yoshikatsu Kanai, Eiji Takeda and Ken-ichi Miyamoto : ) Molecular events involved in up-regulating human Na+-independent neutral amino acid transporter LAT1 during T-cell activation, The Biochemical Journal, Vol.358, No.3, 693-704, 2001. (Keyword) elongation / promoter / run-on assay
104.	Takehisa Yamamoto, Ken-ichi Miyamoto, Keiichi Ozono, Yutaka Taketani, Kanako Katai, Akimitsu Miyauchi, Masaaki Shima, Hideki Yoshikawa, Kosei Yoh, Eiji Takeda and Shintaro Okada : Hypophosphatemic rickets accompanying McCune Albright syndrome: evidence that a humoral factor causes hypophosphatemia, Journal of Bone and Mineral Metabolism, Vol.19, No.5-6, 287-295, 2001. (Summary) McCune-Albright syndrome (MAS) is sometimes complicated by hypophosphatemia. However, it remains unclear whether a humoral factor is associated with the cause of hypophosphatemia. We isolated cells with mutations of the Gsalpha gene from fibrous bone dysplasia tissues of two MAS patients (MAS cells). Severe combined immunodeficiency (SCID) mice were subjected to experiments using from one of these cells patients. Effects of conditioned media (CM) isolated from MAS cells (MAS-CM) on phosphate transport were investigated by using rat renal slices, the renal cell line OK-B, rat intestinal rings and the human intestinal cell line Caco-2. In addition, the effects of MAS-CM on human sodium-dependent phosphate transporter (NPT2) gene promoter activity expression were investigated in the renal cell line OK-B2400 and were compared with the effects of CM isolated from a patient with oncogenic hypophosphatemic osteomalacia (OHO). MAS cells caused significant hypophosphatemia (P < 0.05) and elevated serum alkaline phosphatase activity (P < 0.05) in SCID mice. The MAS-CM significantly inhibited phosphate uptake in everted intestinal rings (P < 0.01), whereas it had no effect on glucose uptake. The MAS-CM had no effect on either phosphate uptake in the kidney or NPT2 gene promoter activity. In contrast, the CM of the OHO patient significantly inhibited phosphate uptake and NPT2 gene promoter activity. These results indicate that the humoral factor derived from fibrous dysplasia cells of the MAS patient is different to that from OHO patients, because the humoral factor from the MAS patient inhibited phosphate transport not in the kidney but in the intestine. (Keyword) Adolescent / Adult / Animals / Bacterial Proteins / Cells, Cultured / Culture Media, Conditioned / Female / Fibrous Dysplasia, Polyostotic / GTP-Binding Protein alpha Subunits, Gs / Hot Temperature / Humans / Hypophosphatemia / Hypophosphatemia, Familial / In Vitro Techniques / Jejunum / Kidney / Membrane Transport Proteins / Mice / Mice, SCID / Phosphates / Promoter Regions, Genetic / Rats / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1007/s007740170012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11498730 ● Search Scopus @ Elsevier (PMID): 11498730 ● Search Scopus @ Elsevier (DOI): 10.1007/s007740170012 (DOI: 10.1007/s007740170012, PubMed: 11498730)
105.	Takeharu Tonai, Kei-ichiro Shiba, Yutaka Taketani, Yasukazu Ohmoto, Kaori Murata, Masahiro Muraguchi, Hiroyuki Ohsaki, Eiji Takeda and Takehiko Nishisho : A neutrophil elastase inhibitor (ONO-5046) reduces neurologic damage after spinal cord injury in rats, Journal of Neurochemistry, Vol.78, No.5, 1064-1072, 2001. (Summary) In view of a cytoprotective effect of elastase inhibitor on chemokine-mediated tissue injury, we examined the neuroprotective effect of ONO-5046, a specific inhibitor of neutrophil elastase, in rats with spinal cord injury. Standardized spinal cord compression markedly increased cytokine-induced neutrophil chemo-attractant (CINC)-1 mRNA and protein. Their increases correlated with neurologic severity of injured rats. Immunohistochemically, CINC-1 protein was detected sequentially in vascular endothelial cells at 4 h, in perivascular neutrophils at 8 h, and in neutrophils infiltrating into cord substance at 12 h. Pretreatment with ONO-5046 (50 mg/kg) markedly ameliorated motor disturbance in injured rats, and reduced CINC-1 protein and mRNA expression. ONO-5046 also significantly reduced the increase of neutrophil accumulation or infiltration estimated by myeloperoxidase activity, and the extent of vascular permeability by Evans blue extravasation in the injured cord segment in comparison to control animals receiving vehicle. These results suggest that CINC-1 contributed to inflammation in rat spinal cord injury and ONO-5046 attenuated neurologic damage partly by blocking CINC-1 production of the chemoattractant, preventing neutrophil activation and vascular endothelial cell injury. (Keyword) Animals / Blood-Brain Barrier / Chemokine CXCL1 / Chemokines, CXC / Chemotactic Factors / Gene Expression / Glycine / Growth Substances / Immunohistochemistry / Intercellular Signaling Peptides and Proteins / Interleukin-8 / Leukocyte Elastase / Motor Activity / Peroxidase / RNA, Messenger / Rats / Rats, Wistar / Recovery of Function / Serine Proteinase Inhibitors / Spinal Cord / Spinal Cord Injuries / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1471-4159.2001.00488.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11553680 ● Search Scopus @ Elsevier (PMID): 11553680 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1471-4159.2001.00488.x (DOI: 10.1046/j.1471-4159.2001.00488.x, PubMed: 11553680)
106.	Tomoko Nii, Yutaka Taketani, Yoshiko Tani, Ichiro Ohkido, Hiroko Segawa, Hitonori Yamamoto, Kyoko Morita, Kanshi Minamitani, Masanori Minagawa, Toshiyuki Yasuda, Hiroo Niimi, Akimitsu Miyauchi, Ken-ichi Miyamoto and Eiji Takeda : Direct demonstration of humorally mediated inhibition of the transcription of phosphate transporter in XLH patients, Clinical and Experimental Nephrology, Vol.5, No.3, 144-152, 2001. (Link to Publication Site) ● Publication site (DOI): 10.1007/s101570170002 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-17944363928 (DOI: 10.1007/s101570170002, Elsevier: Scopus)
107.	Hidekazu Arai, Ken-ichi Miyamoto, Michiko Yoshida, Hironori Yamamoto, Yutaka Taketani, Kyoko Morita, Megumi Kubota, Shigeko Yoshida, Mikiko Ikeda, F Watabe, Y Kanemasa and Eiji Takeda : The polymorphism in the caudal-related homeodomain protein Cdx-2 binding element in the human vitamin D receptor gene, Journal of Bone and Mineral Research, Vol.16, No.7, 1256-1264, 2001.
108.	Megumi Kubota, Shigeko Yoshida, Mikiko Ikeda, Y Okada, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Association between two types of vitamin d receptor gene polymorphism and bone status in premenopausal Japanese women., Calcified Tissue International, Vol.68, No.1, 16-22, 2001. (Link to Publication Site) ● Publication site (DOI): 10.1007/BF02684998 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-0347747812 (DOI: 10.1007/BF02684998, Elsevier: Scopus)
109.	中村多希, Hisami Okumura, 粟根尚美, Eiji Takeda, Akira Mizuno and 田代征記 : 肝硬変患者の耐糖能障害に関するアセスメント, Japanese Journal of Nutritional Assessment, Vol.18, 31-34, 2001. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572824499876027264 (CiNii: 1572824499876027264)
110.	Takamasa Ohnishi, Eiji Takeda, Shiro Yogita, Hidenori Miyake, Takafumi Kinoshita, Yoshiyasu Terashima, Toshio Matsumoto and Seiki Tashiro : Effects of alendronate on bone metastases and hypercarcemia after surgery for hepatocellular carcinoma, Japanese Journal of Clinical Oncology, Vol.30, No.9, 410-413, 2000. (Summary) Alendronate, a bisphosphonate compound, lowers serum calcium in patients with cancer-associated hypercalcemia through its inhibitory effect on bone resorption and as a result symptoms associated with hypercalcemia improve. This study was carried out to investigate the effects of alendronate in patients with hypercalcemia due to bone metastasis of hepatocellular carcinoma (HCC). Two patients were evaluated. Their corrected serum calcium and alpha-fetoprotein (AFP) levels and their computed tomography (CT), bone scintigraphy and magnetic resonance imaging (MRI) findings were evaluated before and during alendronate treatment. After treatment, not only the corrected serum calcium levels but also AFP levels and bone pain decreased; in addition, the regression of the metastatic focus was noted in the MRI analysis. These tumor inhibitory effects of alendronate have not been reported in HCC before; and alendronate might serve to prevent bone metastases in patients with HCC. In conclusion, two patients who developed hypercalcemia associated with bone metastasis after surgery for HCC were treated with alendronate and they experienced alleviation of the pain due to bone metastasis, improvement of their quality of life and a marked decrease in AFP levels with tumor regression. (Keyword) Aged / Alendronate / Bone Neoplasms / Carcinoma, Hepatocellular / Female / Humans / Hypercalcemia / Liver Neoplasms / Male (Link to Publication Site) ● Publication site (DOI): 10.1093/jjco/hyd105 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11095140 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033661348 (DOI: 10.1093/jjco/hyd105, PubMed: 11095140, Elsevier: Scopus)
111.	久野明子, Masaharu Nishi, 岩村利佳子, 横田貴美, Hisami Yamanaka, 田代正記 and Eiji Takeda : 胃切除患者の栄養アセスメント, 日本病態栄養学会誌, Vol.3, 114-127, 2000.
112.	Kanako Katai, Ken-ichi Miyamoto, Sachie Kishida, Hiroko Segawa, Tomoko Nii, Hiroko Tanaka, Yoshiko Tani, Hidekazu Arai, Sawako Tatsumi, Kyoko Morita, Yutaka Taketani and Eiji Takeda : Regulation of intestinal Na+-dependent phosphate co-transporters by a low-phosphate diet and 1,25-dihydroxyvitamin D3., The Journal of Biochemistry, Vol.343, No.3, 705-712, 1999.
113.	Hisami Okumura, Kaori Genjida, Kimi Yokota, Yutaka Taketani, Kyoko Morita, Ken-ichi Miyamoto, Hidenori Miyake, Seiki Tashiro and Eiji Takeda : Daily pattern of energy metabolism in cirrhosis., Nutrition, Vol.15, No.10, 749-754, 1999. (Summary) The daily pattern of energy expenditure and the oxidation rates of carbohydrates, fats, and protein were evaluated by indirect calorimetry in 18 control subjects (Group 1) and 34 cirrhotic patients who were divided into Groups 2a and 2b showing indocyanin green retention rates at 15 min of <30% and 30% or more, respectively. The ratio of resting energy expenditure to basal energy expenditure (%REE) was higher in the cirrhotic patients than in the controls at 8:30 AM and 2:30 PM. The oxidation rates of carbohydrates and fats under fasting conditions in Group 2b patients were respectively lower, and higher than in Group 1 and 2a patients. After the subjects ate, glucose became the substrate preferentially metabolized, and the proportion of fat metabolized was reduced from 82.9+/-5.1% to 43.9+/-21.9% and from 70.7+/-14.1% to 46.8+/-13.9% in the patients with advanced and less advanced cirrhosis, respectively, and from 59.4+/-27.2% to 48.4+/-18.5% in the controls. The fasting concentrations of non-esterified fatty acids in Group 2b were also significantly higher than those in the Group 1 and Group 2a patients. After eating, these concentrations fell and reached similar levels in the patients and controls. These data indicated that the patients with cirrhosis developed the catabolic state of starvation in the morning because of a lack of glycogen stores. Therefore, frequent meal supplementation to prevent early-onset starvation and energy deficiency may be advisable in such patients to maintain a well-nourished condition. (Keyword) Aged / Basal Metabolism / Calorimetry, Indirect / Dietary Carbohydrates / Dietary Fats / Dietary Proteins / energy metabolism / Fasting / Fatty Acids, Nonesterified / Food / Glycogen / Humans / Liver Cirrhosis / Middle Aged / Oxidation-Reduction (Link to Publication Site) ● Publication site (DOI): 10.1016/S0899-9007(99)00149-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10501287 ● Search Scopus @ Elsevier (PMID): 10501287 ● Search Scopus @ Elsevier (DOI): 10.1016/S0899-9007(99)00149-5 (DOI: 10.1016/S0899-9007(99)00149-5, PubMed: 10501287)
114.	Hisami Okumura, Eiji Takeda, Kazumi Takata, Emi Shuto, Ken-ichi Miyamoto, Toshiyuki Watanabe, Yoshifumi Kawano, Yoichi Takaue and Yasuhiro Kuroda : Total parenteral nutrition on energy metabolism in children undergoing autologous peripheral blood stem cell transplantation., The Journal of Medical Investigation : JMI, Vol.44, No.3-4, 199-203, 1998. (Summary) The resting energy expenditure (REE) and the respiratory quotient (RQ) were measured longitudinally using indirect calorimetry to examine the effects of total parenteral nutrition (TPN) on energy metabolism in children undergoing autologous peripheral blood stem cell transplantation (PBSCT). There were six children (two males and four females) and the age ranged from five to 13 years (median, eight yrs). The diagnosis included acute lymphocytic leukemia (ALL; 4), neuroblastoma (NBL; 1) and primitive neuroectodermal tumor (PNET; 1). TPN was started after the patients were stabilized following PBSCT (group A; n = 3) or before the initiation of high-dose cytoreductive chemotherapy (HCC) (group B; n = 3). Duration of HCC before PBSCT was identical between the two groups (six to eight days). Average total calorie and protein intake during HCC was significantly higher for group B than for group A. The %REE, the percentage of REE to the predicted basal energy expenditure (BEE), in group A showed 133 +/- 19%, 129 +/- 14% and 146 +/- 11% during three periods of HCC (days -8 to -1 of PBSCT), bone marrow suppression (days 0 to 11 of PBSCT) and bone marrow recovery (days 12 to 22 of PBSCT), respectively. In contrast, those in group B were 10% to 20% lower than those in group A at all periods. Carbohydrate oxidation rates during HCC in group A were significantly lower than those in group B, and those were not different between both groups during post-PBSCT periods. Fat oxidation rates in both groups were similar at all stages of periods. In contrast, protein degradation rates in group A were significantly higher than those in group B at all stages of the period. From these results, we concluded that commencement of TPN administration prior to HCC in the patients undergoing PBSCT provides beneficial effects to maintain better energy metabolic and nutritional status. (Keyword) Adolescent / Child / Child, Preschool / energy metabolism / Female / Hematopoietic Stem Cell Transplantation / Humans / Male / Parenteral Nutrition / Transplantation, Autologous (Tokushima University Institutional Repository) ● Metadata: 110667 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9597809 ● Summary page in Scopus @ Elsevier: 2-s2.0-0031995075 (Tokushima University Institutional Repository: 110667, PubMed: 9597809, Elsevier: Scopus)
115.	Kazumi Takata, Noriko Chiba, Mariko Tawara, Hisami Okumura, Emi Shuto, Ken-ichi Miyamoto, Ichiro Yokota, Junko Matsuda, Yasuhiro Kuroda and Eiji Takeda : Comparison of energy metabolism in insulin-dependent and non-insulin-dependent diabetes mellitus, The Journal of Medical Investigation : JMI, Vol.44, No.1-2, 67-71, 1997. (Summary) To compare the metabolic consequences of insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), glycemic control and energy metabolism were evaluated in 18 children displaying IDDM and 19 NIDDM adult patients. With rising concentrations of fasting blood glucose (FBG), hemoglobin A1C and free fatty acid, the percentage of the ratio of resting energy expenditure (REE) to predicted REE expressed as %REE increased and the respiratory quotient (RQ) decreased. The linear regression between RQ and FBG showed the same gradient in IDDM and NIDDM although the RQ in IDDM was always 0.07 lower than that in NIDDM given various FBG concentrations. Those patients whose RQ values were less than 0.7, indicating ketone body production, included 8 (44%) IDDM and 2 (11%) NIDDM patients. These results may explain the relatively greater manifestation of ketoacidosis in IDDM. (Keyword) Adult / Child / Diabetes Mellitus, Type 1 / Diabetes Mellitus, Type 2 / energy metabolism / Humans / Middle Aged (Tokushima University Institutional Repository) ● Metadata: 111643 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9395720 ● Summary page in Scopus @ Elsevier: 2-s2.0-0031196541 (Tokushima University Institutional Repository: 111643, PubMed: 9395720, Elsevier: Scopus)
116.	Hidekazu Arai, Ken-ichi Miyamoto, Yutaka Taketani, Hironori Yamamoto, Yuka Iemori, Kyoko Morita, Takeharu Tonai, Takehiko Nishisho, Shigenobu Mori and Eiji Takeda : A vitamin D receptor gene polymorphism in the translation initiation codon: effect on protein activity and relation to bone mineral density in Japanese women., Journal of Bone and Mineral Research, Vol.12, No.6, 915-921, 1997.
117.	Kanako Katai, Hiroko Segawa, Hiromi Sakata-Haga, Kyoko Morita, Hidekazu Arai, Sawako Tatsumi, Yutaka Taketani, Ken-ichi Miyamoto, Setsuji Hisano, Yoshihiro Fukui and Eiji Takeda : Acute regulation by dietary phosphate of the sodium-dependent phosphate transporter (NaP(i)-2) in rat kidney., The Journal of Biochemistry, Vol.121, No.1, 50-55, 1997.
118.	Eiji Takeda, K. Takata, H. Yamanaka, Yutaka Taketani, K. Morita, Ken-ichi Miyamoto, Masayuki Shono, S. Teshima and Kazuhito Rokutan : Vitamin D3 elicits calcium response and activates blood monocyte-derived macrophages from patients with vitamin D dependent rickets type II., FEBS Letters, Vol.4, No.364, 157-160, 1996. (Keyword) Vitamin D3 / monocyte
119.	Eiji Takeda, Kazumi Takata, Hisami Yamanaka, Yutaka Taketani, Kyoko Morita, Ken-ichi Miyamoto, Masayuki Shono, Shigetada Teshima and Kazuhito Rokutan : Vitamin D3 elicits calcium response and activates blood monocyte-derived macrophages from patients with vitamin D dependent rickets type 2, FEBS Letters, Vol.396, 157-160, 1996. (Keyword) vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release
120.	Eiji Takeda, Kazumi Takata, Hisami Yamanaka, Yutaka Taketani, Kyoko Morita, Ken-ichi Miyamoto, Masayuki Shono, Shigetada Teshima and Kazuhito Rokutan : Vitamin D3 elicits calcium response and activates blood monocyte-derived macrophages from patients with vitamin D dependent rickets type 2, FEBS Letters, Vol.396, 157-160, 1996. (Keyword) vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release
121.	Yasunobu Hayabuchi, Eiji Takeda, 伊藤道徳, Takahiko Saijyou, Etsuo Naito, Junko Matsuda, マーブブルホク and Yasuhiro Kuroda : 関節痛により発見されたマンノシドーシスの姉妹例, 日本小児科学会雑誌, Vol.95, No.7, 1666-1671, 1991.

Academic Paper (Unrefereed Paper):

1.	Nozomi Yokoyama, Hironori Yamamoto, Yutaka Taketani, Masayuki Iwano and Eiji Takeda : Association with Fetuin-A and Ectopic Calcification in -Klotho Mutant Mice., American Society of Nephrology Kidney Week 2013, Atlanta, USA, 2013.
2.	Hisami Okumura, 足立知咲, 周蓓 and Eiji Takeda : 無理なくダイエット!∼ボリュメトリクス∼エネルギー密度(ED)に注目した低エネルギーでも満腹度・満足度の高い昼食の検討, New Food Industry, Vol.55, No.5, 17-24, 2013.
3.	Hisami Okumura, 山内利香, 浦野恵理, 寺本有沙, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : 肝硬変患者に対するテーラーメイド栄養管理の血液生化学指標についての検討, 栄養アセスメント, Vol.28, No.1, 18-20, 2011.
4.	Eiji Takeda, Hironori Yamamoto, Yuka Nishida, Tadatoshi Sato, Naoki Sawada and Yutaka Taketani : Phosphate restriction in diet therapy., Contributions to Nephrology, Vol.155, 113-124, 2007. (Summary) Hyperphosphatemia and hyperparathyroidism, frequently observed in patients with endstage renal disease, are associated with renal osteodystrophy, organ calcification, cardiovascular disease and sudden death. Restriction of dietary protein and phosphorus is beneficial in slowing the progression of renal failure. Dietary phosphorus restriction must be prescribed at all stages of renal failure in adults. It may be achieved by decreasing protein intake and avoiding foods rich in phosphorus. An average of 60-80% of the phosphorus intake is absorbed in the gut in dialysis patients. If phosphate binders are employed, the phosphorus absorbed from the diet may be reduced to 40%. Conventional hemodialysis with a high-flux, high-efficiency dialyzer removes approximately 30 mmol (900 mg) phosphorus during each dialysis performed three times weekly. Therefore, 750 mg of phosphorus intake should be the critical value above which a positive balance of phosphorus may occur. This value corresponds to a protein diet of 45-50 g/day or 0.8 g/kg body weight/day for a 60 kg patient. Target levels should become 9.2-9.6 mg/dl for calcium, 2.5-5.5 mg/dl for phosphorus, <55 mg2/dl2 for the calcium-phosphorus product, and 100-200 pg/ml for intact parathyroid hormone. (Keyword) Diet Therapy / Dietary Proteins / Disease Progression / Food, Formulated / Humans / Kidney Failure, Chronic / Phosphates / Phosphorus, Dietary / Renal Osteodystrophy (Link to Publication Site) ● Publication site (DOI): 10.1159/000101004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17369719 ● Search Scopus @ Elsevier (PMID): 17369719 ● Search Scopus @ Elsevier (DOI): 10.1159/000101004 (DOI: 10.1159/000101004, PubMed: 17369719)
5.	Eiji Takeda, Hidekazu Arai, Kazusa Muto, Kaoru Matsuo, Masae Sakuma, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Gene expression in low glycemic index diet - impact on metabolic control., Forum of Nutrition, Vol.60, 127-139, 2007. (Summary) Correcting postprandial hyperglycemia forms an important part of the prevention and management of type 2 diabetes. A low-glycemic-index liquid formula designated as Inslow was prepared by replacing dextrin in the standard balanced formula (SBF) with 55.7% palatinose. Long-term administration of Inslow prevented fatty liver and improved insulin resistance in rats. Expressions of mRNA of factors involved in glucose and lipid metabolism were determined to clarify its mechanism. Analysis of mRNA expressions revealed that Inslow increased the expression of enzymes involved in Beta -oxidation and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) in the liver, and increased PPAR-gamma, adiponectin and uncoupling protein 2 as well as decreased tumor necrosis factor alpha in adipose tissue in comparison with those of SBF. Inslow may induce improvement of insulin resistance by accelerated Beta-oxidation through increased expression of the hepatic PPAR-alpha gene and adipocyte PPAR-gamma gene. Therefore, Inslow is a functional food which prevents and treats type 2 diabetes. (Keyword) Animals / Diabetes Mellitus, Type 2 / Disease Models, Animal / Gene Expression Regulation / Glycemic Index / Humans / Oxidative Stress / PPAR alpha / PPAR gamma / Postprandial Period (Link to Publication Site) ● Publication site (DOI): 10.1159/000107089 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17684409 ● Search Scopus @ Elsevier (PMID): 17684409 ● Search Scopus @ Elsevier (DOI): 10.1159/000107089 (DOI: 10.1159/000107089, PubMed: 17684409)
6.	Hisami Okumura, 谷口章子, 浪花裕子, 西田由香, 竹内晴美, 佐久間理英, 谷佳子, Yasuko Takahashi and Eiji Takeda : 粘性食を組み合わせた朝食長期摂取によるインスリン感受性，脂質代謝改善評価, 栄養-評価と治療, Vol.23, No.6, 40-43, 2006.
7.	谷口章子, Hisami Okumura, 西田由香, Hironori Yamamoto and Eiji Takeda : 粘性食品を組み合わせた朝食摂取の血糖およびインスリン反応への効果, 栄養-評価と治療, Vol.22, 69-77, 2005.
8.	竹内晴美, Hisami Okumura, 中村多希, 竹内里美, Hidekazu Arai, Yutaka Taketani, Masahiko Fujii, Hidenori Miyake, 田代正記 and Eiji Takeda : SF-36を用いた肝硬変患者におけるLES療法長期継続効果の検討, 栄養-評価と治療, Vol.21, 573-577, 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570291226541281920 (CiNii: 1570291226541281920)
9.	横田貴美, 源氏田可織, Hisami Yamanaka, Kyoko Morita, 篠原麻衣子, 坂本恭子, Eiji Takeda, Hidenori Miyake and 田代正記 : 肝硬変患者の栄養代謝アセスメント, 栄養-評価と治療, Vol.15, No.4, 385-389, 1998.

Review, Commentary:

1.	Eiji Takeda, Hironori Yamamoto and Yutaka Taketani : Phosphate as a novel signal in the intracellular signal transduction, Vitamins, Vol.89, No.8, 393-396, Aug. 2015. (Summary) The phosphate (Pi)-mediated signal transduction pathways in renal proximal tubular cells and endothelial cells were examined, because Pi depletion and overloading are known to influence gene expression and cellular function. In renal proximal tubular calls (LLC-PK1), Pi depletion resulted in increases in intracellular inositol triphosphate (IP3) and calcium ion (Ca^<2+>) levels, the latter of which may be associated with the maintenance of Pi homeostasis. On the other hand, exposing bovine aortic endothelial cells to excessive Pi load increased production of reactive oxygen species, which depended on phosphorus influx via sodium-dependent phosphate transporters, and decreased nitric oxide production via inhibitory phosphorylation of endothelial nitric oxide synthase. Pi loading in rat aortic rings inhibited endothelium-dependent vasodilation. A high dietary Pi load in human subjects increased serum Pi level at 2 h and significantly decreased flow-mediated dilation. Thus, it was found that the function of endothelial cells was damaged by the high dietary Pi loading. Taken together, these findings suggest that the changes in serum Pi level are associated with human health by affecting the intracellular Pi signal transduction pathway. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205701585536 (CiNii: 1390001205701585536)
2.	Eiji Takeda, Hironori Yamamoto and Yutaka Taketani : 新規シグナルとしてのリン酸, Vitamins, Vol.89, No.8, 393-396, Aug. 2015.
3.	Eiji Takeda, Hisami Okumura, Yutaka Taketani and Hironori Yamamoto : Nutritional science of vitamin D in pediatric and adult diseases, Vitamins, Vol.88, No.10, 499-506, Oct. 2014. (Summary) Nutritional science of vitamin D in pediatric and adult diseases was summarized. Vitamin D-dependency type II is a rare disease caused by a disorder of the human vitamin D receptor (VDR). Except for the alopecia, severe rickets and other biochemical abnormalities of 6 patients were reversed by treatment with 3 g/kg/d of 1-hydroxyvitamin D_3. A polymorphism at the translation initiation codon of the human VDR gene also affects the bone mineral density (BMD) in Japanese. Attention to phosphorus intake is important because both phosphorus deficiency and overloading impair bone health and quality of life (QOL). Elevation of extracellular phosphorus level causes endothelial dysfunction and medial calcification, which are closely associated with the development of cardiovascular disease (CVD). A dietary approach to limit phosphorus intake is particularly important to prevent bone impairment and CVD in patients with chronic kidney disease (CKD). Increased serum fibroblast growth factor 23 (FGF23)level is an early finding of abnormal mineral metabolism in CKD which causes secondary hyperparathyroidism and resistance of the parathyroid gland to the action of FGF23. In order to improve bone health and QOL in the general population, it should be important that attention to phosphorous intake from processed foods containing phosphorus additive is paied. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680676820096 (CiNii: 1390282680676820096)
4.	Eiji Takeda, Hisami Okumura, Yutaka Taketani and Hironori Yamamoto : 小児疾患および成人からみたビタミンD栄養学, Vitamins, Vol.10, 499-506, 2014.
5.	Hisami Okumura, 大南博和, Yutaka Taketani and Eiji Takeda : 「日本食」の食卓を科学的に評価する③ニュートリゲノミクスを用いた日本食の評価, PRACTICE, Vol.31, No.3, 31-34, 2014.
6.	Hisami Okumura, 足立知咲, 周蓓, Yutaka Taketani and Eiji Takeda : 「日本食」の食卓を科学的に評価する②日本食を用いたボリュメトリクス(Volumetrics):エネルギー密度(ED)に注目した低エネルギーでも満腹度・満足度の高い食事, PRACTICE, Vol.31, No.2, 159-163, 2014.
7.	Hisami Okumura, Yutaka Taketani and Eiji Takeda : 「日本食」の食卓を科学的に評価する①食後高血糖を抑制する食事, PRACTICE, Vol.31, No.1, 31-34, 2014.
8.	中尾真理, Hironori Yamamoto, 中橋乙起, 阿部航太郎, Yutaka Taketani and Eiji Takeda : 慢性腎不全時のリン制限食を用いた栄養療法は，腎性貧血の発症進展を予防する, Shikoku Acta Medica, Vol.68, No.5-6, 270-271, Dec. 2012.
9.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : リンの栄養学健康と疾患(解説), 香川県小児科医会会誌, No.33, 35-39, Jun. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523106605284363136 (CiNii: 1523106605284363136)
10.	Eiji Takeda, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Depression and nutrition, Shikoku Acta Medica, Vol.68, No.1, 3-8, Apr. 2012. (Summary) Severe and prolonged stress exposure impairs homeostatic mechanisms, particularly associatedwith the onset of depressive illness. Brain food is aimed at preventing as well as treating a growingnumber of depression. An increase in brain tryptophan levels on the order of that produced byeating a carbohydrate-rich/protein-poor meal causes parallel increases in the amounts of serotoninreleased into synapses. Dietary antioxidants present in fruits and vegetables may also improvemood. Furthermore, lifestyle of breakfast, lunch and dinner with family or friends is a very importantfactor to reduce depression. (Tokushima University Institutional Repository) ● Metadata: 97911 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287417308416 (Tokushima University Institutional Repository: 97911, CiNii: 1050564287417308416)
11.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : 栄養素輸送システムと食品機能, 消化と吸収, Vol.34, No.2, 11-19, Feb. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572824500597643264 (CiNii: 1572824500597643264)
12.	Eiji Takeda, 谷佳子 and Hisami Okumura : 臨床栄養管理の意義とエビデンス，臨床栄養管理法―栄養アセスメントから経済評価まで―, 建帛社, 38, May 2011.
13.	Hisami Okumura, 川上由香, 佐久間理英 and Eiji Takeda : 大麦を利用した食後高血糖抑制割合の検討と食品評価, New food industry, Vol.53, No.4, 12-22, Apr. 2011. (Keyword) 大麦 / 食後高血糖 / GI値 / ニュートリゲノミクス / DNAチップ解析 / 食事療法 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522825129865280000 (CiNii: 1522825129865280000)
14.	Eiji Takeda, 谷村綾子 and 増田真志 : 内科医のための骨粗鬆症・カルシウム・リン代謝からあらためて骨を考える, Mebio, No.8, 12-17, Aug. 2008.
15.	Yutaka Taketani, Hironori Yamamoto, Eiji Takeda and Ken-ichi Miyamoto : Vitamin D and phosphate metabolism, --- relationship with aging-regulating gene ---, CLINICAL CALCIUM, Vol.16, No.7, 1137-1142, Jul. 2006.
16.	Eiji Takeda : 痛風・高尿酸血症, 栄養・食糧学データハンドブック, 343, Jan. 2006.
17.	Eiji Takeda : 第6章ストレス制御をめざす栄養科学, 食品機能素材Ⅲ, 54-59, Nov. 2005.
18.	Eiji Takeda, 西田由香 and 竹内晴美 : 痛風・高尿酸血症, 診断と治療, Vol.93, No.10, 1747-1750, Oct. 2005.
19.	川浦昭彦, 西田由香 and Eiji Takeda : リン摂取と骨密度, Clinical Calcium, Vol.15, No.9, 55-60, Sep. 2005.
20.	Eiji Takeda : 座談会・経腸栄養の素材と生体機能調節, Japanese Journal of Nutritional Assessment, Vol.22, No.4, 81-89, Aug. 2005.
21.	Eiji Takeda : 先天性代謝異常, 健康・栄養科学シリーズ人体の構造と機能及び疾病の成り立ち各論Ⅰ, 85-88, May 2005.
22.	Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : ビタミンDレセプター遺伝子多型と骨代謝, 臨床栄養, Vol.106, No.5, 580-586, May 2005.
23.	Eiji Takeda : 分子栄養学とは? 食事で遺伝子の発現が変わるのか?, Japanese Journal of Pediatric Medicine, Vol.37, No.5, 608-609, May 2005.
24.	Eiji Takeda : ストレス制御をめざす栄養科学, 日本学術会議中国・四国地区ニュース, No.38, Mar. 2005.
25.	Kimie Nakagawa, Akihiko Kawaura, Shigeaki Kato, Eiji Takeda and Toshio Okano : 1α,25-Dihydroxyvitamin D₃ is a preventive factor in the metastasis of lung cancer, Carcinogenesis, Vol.26, No.2, 429-440, Feb. 2005. (Summary) 1alpha,25-Dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)], the major regulator of calcium homeostasis, has potent antiproliferative and anti-invasive properties in vitro in cancer cells. Studies in vivo demonstrated that 1alpha,25(OH)(2)D(3) slows the progression of breast, prostate and other carcinomas. A key question is whether 1alpha,25(OH)(2)D(3) exerts its anticarcinogenic effects in vivo by a mechanism that is dependent on its capacity to limit the proliferation and invasiveness of cancer cells in vitro. It has not been clear whether the calcemic activity and regulation of the host defenses by 1alpha,25(OH)(2)D(3) contribute to the effect on cancer cells. In this study we have focused on the influence of 1alpha,25(OH)(2)D(3) on the metastasis of lung cancer, without involvement of the calcemic activity and other effects of 1alpha,25(OH)(2)D(3) in the host. We used metastatic Lewis lung carcinoma cells expressing green fluorescent protein (LLC-GFP cells) and examined metastatic activity in vitamin D receptor (VDR) null mutant (VDR(-/-)) mice and their wild-type counterparts (VDR(+/+) mice). VDR(-/-) mice exhibit hypocalcemia and extremely high serum levels of 1alpha,25(OH)(2)D(3). We expected that serum 1alpha,25(OH)(2)D(3) would act in vivo to directly inhibit the metastatic growth of VDR-positive LLC-GFP cells in VDR(-/-) mice. The metastatic activities of LLC-GFP cells were remarkably reduced in VDR(-/-) mice compared with VDR(+/+) mice. To test the hypothesis that serum 1alpha,25(OH)(2)D(3) is an intrinsic factor that inhibits metastatic growth of lung cancer cells, we corrected hypocalcemia and/or hypervitaminosis D in VDR(-/-) mice by dietary manipulation. The metastatic growth of LLC-GFP cells was remarkably reduced in response to serum levels of 1alpha,25(OH)(2)D(3), but not to serum calcium levels. Furthermore, we found that VDR(+/+) mice fed the manipulated diets displayed an apparent inverse relationship between the physiological levels of serum 1alpha,25(OH)(2)D(3) (8-15 pg/ml) and tumorigenesis. Here we show that 1alpha,25(OH)(2)D(3) inhibits the metastatic growth of lung cancer cells in a defined animal model. (Keyword) Animals / calcium / Cell Proliferation / Diet / Green Fluorescent Proteins / Hypocalcemia / Lung Neoplasms / Mice / knockout mice / Receptors, Calcitriol / Tumor Cells, Cultured / Vitamin D (Link to Publication Site) ● Publication site (DOI): 10.1093/carcin/bgh332 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15539405 ● Summary page in Scopus @ Elsevier: 2-s2.0-13844266142 (DOI: 10.1093/carcin/bgh332, PubMed: 15539405, Elsevier: Scopus)
26.	Eiji Takeda : 臨床栄養管理, ILSI, Vol.84, 14-21, 2005.
27.	Eiji Takeda, Hisami Okumura and Yutaka Taketani : 特集「透析患者の栄養評価における新理論と新技術」Ⅰ総論:最近の栄養評価における理論と技術およびその問題点, 臨牀透析, Vol.20, No.12, 7-14, Jul. 2004.
28.	Eiji Takeda and Yutaka Taketani : 特集 - エビデンスからみた機能性食品の現状 2. 耐糖能改善食品(1)食物繊維, 栄養評価と治療, Vol.21, No.3, 237-240, Jun. 2004.
29.	Eiji Takeda and Yutaka Taketani : 生体におけるリンの役割と制御, 腎不全とリン, 17-21, Jun. 2004.
30.	Eiji Takeda : III 食事療法肝疾患合併時, 糖尿病最新の治療 2004-2006, 84-85, Feb. 2004.
31.	Eiji Takeda : 小児のこころと身体の健康を支援する栄養科学, 大阪府学校医会誌, No.28, 1-12, 2004.
32.	Eiji Takeda : 炎症性腸疾患に対する栄養管理の進歩, 消化と吸収, Vol.27, No.1, 20-23, 2004.
33.	Eiji Takeda, Yutaka Taketani, Naoki Sawada, Tadatoshi Sato and Hironori Yamamoto : The regulation and function of phosphate in the human body, BioFactors, Vol.21, No.1-4, 345-355, 2004. (Summary) Inorganic phosphate (Pi) is required for cellular function and skeletal mineralization. Serum Pi level is maintained within a narrow range through a complex interplay between intestinal absorption, exchange with intracellular and bone storage pools, and renal tubular reabsorption. Pi is abundant in the diet, and intestinal absorption of Pi is efficient and minimally regulated. The kidney is a major regulator of Pi homeostasis and can increase or decrease its Pi reabsorptive capacity to accommodate Pi need. The crucial regulated step in Pi homeostasis is the transport of Pi across the renal proximal tubule. Type II sodium-dependent phosphate (Na/Pi) cotransporter (NPT2) is the major molecule in the renal proximal tubule and is regulated by hormones and nonhormonal factors. Recent studies of inherited and acquired hypophosphatemia which exhibit similar biochemical and clinical features, have led to the identification of novel genes, phosphate regulating gene with homologies to endopeptidases on the X chromosome (PHEX) and fibroblast growth factor-23 (FGF-23), that play a role in the regulation of Pi homeostasis. The PHEX gene encodes an endopeptidase, predominantly expressed in bone and teeth but not in kidney. FGF-23 may be a substrate of this endopeptidase and inhibit renal Pi reabsorption. In a survey in the United States and in Japan, the amount of phosphorus from food is gradually increasing. It is thought that excess amounts of phosphorus intake for long periods are a strong factor in bone impairment and ageing. The restriction of phosphorus intake seems to be important under low calcium intake to keep QOL on high level. (Keyword) Aging / Chromosome Mapping / Chromosomes, Human / Chromosomes, Human, X / Humans / Hypophosphatemia, Familial / Phosphates / Quality of Life / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type I / Sodium-Phosphate Cotransporter Proteins, Type II / Sodium-Phosphate Cotransporter Proteins, Type III / Symporters (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15630224 ● Summary page in Scopus @ Elsevier: 2-s2.0-16444386966 (PubMed: 15630224, Elsevier: Scopus)
34.	Hironori Yamamoto, 佐藤匡俊, 澤田直樹 and Eiji Takeda : Ⅶ．骨粗鬆症ビタミンD至適摂取量-活性型ビタミンDを使用した場合の対応も含めて, Clinical Calcium, Vol.14, No.1, 56-59, Dec. 2003.
35.	Eiji Takeda, Hidekazu Arai and Yutaka Taketani : 分子栄養学からみた糖尿病の予防と治療, 臨床栄養, Vol.103, No.5, 565-569, Oct. 2003.
36.	Eiji Takeda and 山本良郎 : 生体での栄養代謝調節, 栄養食品学-基礎と応用-, 272-309, Oct. 2003.
37.	Eiji Takeda, Yutaka Taketani and 三宅秀則 : 肝疾患における低栄養の病態と治療, KAN TAN SUI, Vol.47, No.1, 93-98, Jul. 2003.
38.	Eiji Takeda : 小児の栄養, 標準小児科学第5版, 23-37, Mar. 2003.
39.	Eiji Takeda : ビタミン欠乏症微量元素欠乏症, 内科学第8版, Vol.8, No.1, 1765-1769, Mar. 2003.
40.	Yutaka Taketani and Eiji Takeda : 重症心身障害児の至適投与熱量と栄養基質, JJPEN輸液栄養, Vol.25, No.2, 63-67, Feb. 2003.
41.	Eiji Takeda, 梨木邦剛 and Yutaka Taketani : ミネラルの生体での代謝と吸収, FOOD Style 21, Vol.7, No.2, 41-46, Feb. 2003.
42.	Eiji Takeda and 佐々木一 : 耐糖能障害を予防・改善する機能性食品の開発, 消化と吸収, Vol.26, No.1, 94-97, 2003.
43.	Hisami Okumura, 中村多希, 津田紀子, Yutaka Taketani, 國清紀子, 高橋保子 and Eiji Takeda : 肝硬変の栄養療法-夜食による早朝空腹時のエネルギー代謝改善効果-, 日本病態栄養学会誌, Vol.6, No.1, 17-20, 2003.
44.	粟根尚美, Hidekazu Arai, Eiji Takeda, 松村晃子 and 高橋保子 : 低Glycemic Index食品は2型糖尿病の発症を予防し治療効果を有する, Shikoku Acta Medica, Vol.58, No.4-5, 194-200, Oct. 2002. (Tokushima University Institutional Repository) ● Metadata: 110551 (Tokushima University Institutional Repository: 110551)
45.	Eiji Takeda : 先天性異常症, 食生活, Vol.96, No.10, 82-86, Oct. 2002.
46.	Eiji Takeda : 栄養と遺伝子発現, Journal of Clinical and Experimental Medicine, Vol.202, No.12, 983, Sep. 2002.
47.	Eiji Takeda : 腎尿細管・消化吸収機能異常症, 小児科学第2版, 343-347, Jun. 2002.
48.	渡辺明治, Eiji Takeda, 清野裕 and 立川倶子 : 「病態栄養専門士」とその認定制度, The Japanese Journal of Clinical Nutrition, Vol.100, No.6, 675-679, May 2002. (Keyword) 病態栄養専門士 / 日本病態栄養学会 / TNT研修 / 認定制度 / 栄養スペシャリスト
49.	Eiji Takeda : 病態栄養士をめざすもの, 認定病態栄養士のための病態栄養ガイドブック, 10-13, Mar. 2002.
50.	Eiji Takeda, Hidekazu Arai and Hironori Yamamoto : ヒトビタミンD受容体の腸管での発現と骨粗鬆症, 臨床栄養Update 生活習慣と消化器疾患, Vol.39, No.2, 320-321, Feb. 2002.
51.	Yutaka Taketani, 梨木邦剛, 一色政志 and Eiji Takeda : カルシウム・リン酸輸送とカベオラ, 腎と骨代謝, Vol.15, No.4, 343-349, 2002. (Keyword) カベオラ / カルシウム / リン酸 / トランスポーター / エンドサイトーシス
52.	Yutaka Taketani, 大久保公美, 小林くみ and Eiji Takeda : 炎症性腸疾患の栄養アセスメント, 日本病態栄養学会誌, Vol.5, No.1, 45-48, 2002.
53.	Eiji Takeda, 飯田めぐみ and 小林くみ : リン輸送体の分子生物学, 腎と骨代謝, Vol.15, No.1, 33-38, 2002.
54.	Eiji Takeda, Kyoko Morita, Yutaka Taketani, Hironori Yamamoto and Ken-ichi Miyamoto : Renal handling of phosphate, Calcium In Internal Medicine, 137-148, 2002.
55.	Kyoko Morita, Megumi Iida and Eiji Takeda : Parathyroid Hormone-Mediated Regulation of Renal Phosphate Co-Transporter, CLINICAL CALCIUM, Vol.11, No.12, 82-86, Dec. 2001. (Summary) PTHは，IIa 型リントランスポーターのエンドサイトーシスを誘導することによって腎臓のリン再吸収を抑制する．PTHは刷子縁膜および基底膜に局在するPTH受容体を介して，PKAあるいはPKCの活性化を促進する．これらのシグナル伝達の活性化は，直接NPT2をリン酸化するのではなく，エンドサイトーシスに関連する分子がPTHの作用に重要な役割を果たしていると考えられる．
56.	Eiji Takeda : ビタミンD欠乏性くる病とビタミンD依存性くる病, 小児疾患の診断治療基準, Vol.33, 196-197, Nov. 2001. (Keyword) ビタミンD欠乏症 / ビタミンD依存症I型 / ビタミンD依存症II型
57.	Eiji Takeda, Hidekazu Arai and Kyoko Morita : エネルギー, The Japanese Journal of Clinical Nutrition, Vol.99, No.5, 546-549, Oct. 2001.
58.	Eiji Takeda and Kyoko Morita : 食物成分と薬剤との相互作用, The Lipid, Vol.12, No.5, 59-63, Oct. 2001.
59.	Eiji Takeda : 高齢者栄養学, おいしいね, Vol.12, 15, Jul. 2001.
60.	Eiji Takeda : 骨粗鬆症のリスクファクターである日本人リン摂取過剰に関する研究, 医学研究報告書, 76-79, Jun. 2001.
61.	Eiji Takeda, 野本真由美 and Hironori Yamamoto : ビタミンA,D, The Journal of Pediatric Practice, Vol.64, No.5, 660-665, May 2001.
62.	Eiji Takeda and 加藤秀夫 : 高齢者の食と栄養管理に関する対策と提言, 高齢者の食と栄養管理, 33-57, May 2001.
63.	Eiji Takeda : 高齢者栄養学, おいしいね, Vol.11, 13, May 2001.
64.	Eiji Takeda : 医師のための糖尿病栄養学, メディカルジャーナルDITN, Vol.278, 2-3, Apr. 2001.
65.	Eiji Takeda : リン酸代謝の栄養学, カルシウムと骨, 146-150, Apr. 2001.
66.	Eiji Takeda, 岸田祐枝 and 藤田裕之 : 骨代謝の基礎と最近の知見, Japanese Journal of Pediatric Medicine, Vol.33, No.2, 156-160, Feb. 2001.
67.	Eiji Takeda : 新生児肝炎, 治療指針今日の治療指針 - 私はこう治療している, 825-826, Jan. 2001.
68.	Eiji Takeda : リンの生理機能, HEALTH DIGEST, Vol.16, 1-6, 2001.
69.	Eiji Takeda, Hidekazu Arai, Hisami Yamanaka and Kyoko Morita : ビタミンD受容体遺伝子多型からみた骨粗鬆症に対する栄養管理, 日本臨床栄養学会雑誌, Vol.23, 3-6, 2001.
70.	Hisami Yamanaka, 田口華代 and Eiji Takeda : 肝硬変患者のエネルギー代謝の評価法, JJPEN, Vol.23, No.2, 83-86, 2001.
71.	Eiji Takeda : ビタミンD依存症Ⅱ型, ビタミンD Update 2001, 200-211, 2001.
72.	Eiji Takeda and Hisami Yamanaka : 肝疾患と病態栄養-予防と治療を考える-, 最新肝臓病学全国現状調査から将来展望まで, 110-113, 2001.
73.	Hisami Yamanaka, 篠原麻衣子, 坂本恭子, 横田貴美 and Eiji Takeda : エネルギー代謝からみた肝硬変患者の栄養管理-肝硬変患者のエネルギー代謝, 日本病態栄養学会, Vol.3, 35-43, 2000.

Proceeding of International Conference:

1.	Masashi Masuda, Hironori Yamamoto, Yuichiro Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani : All-trans-retinoic-acid reduces intestinal phosphate uptake by the transcriptional regulation of sodium-dependent phosphate co-transporter gene (Npt2b)., ASBMR 2019 Annual Meeting, Sep. 2019.
2.	Hisami Okumura, Shoko Wada, Takafumi Katayama, Satoru Imura, Yuji Morine, Mitsuo Shimada and Eiji Takeda : Effect of hepatectomy on energy metabolism in patients with liver cancer and cholangiocalcinoma by the difference of resection volume, 38th European Congress for Nutrition and Metabolism, Copenhagen, Sep. 2016.
3.	Hisami Okumura, Akiyoshi Hirayama, Hiroshi Tatano, Tomoyoshi Soga, Masaru Tomita and Eiji Takeda : Serum metabolites and gene expression profiling in peripheral white blood cells in response to the food intake with different glycemic index, 11th Metabolomics Society Conference, San Francisco, CA, USA, Jun. 2015.
4.	Abuduli Maerjianghan, Ohminami Hirokazu, Tamaki Otani, Kubo Hiroshi, Ueda Haruka, Eiji Takeda and Yutaka Taketani : Effect of Dietary Phosphate on Glucose Metabolism by 18F-FDG PET/CT in Rats, 75th Scientific Sessions, American Diabetes Association, Boston Convenstion and Exhibition Center, Boston MA, June 5-9, 2015, Jun. 2015.
5.	Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto : Niacin and Chronic Kidney Disease., ACN2015 Asian Congress of Nutrition., May 2015.
6.	S Wada, Hisami Okumura, B Zhou, Yutaka Taketani, Takafumi Katayama, Yusuke Arakawa, Satoru Imura, Mitsuo Shimada and Eiji Takeda : Effect of hepatectomy on energy metabolism in patients with liver cancer and cholangiocarcinoma by the difference of resection volume, 12th Asian Congress of Nutrition (ACN), May 2015.
7.	H tatano, Hisami Okumura, B Zhou, Yutaka Taketani, Takafumi Katayama and Eiji Takeda : Desire for protein and sweetness is stimulated by dietary habits of high fat intake, 12th Asian Congress of Nutrition (ACN), May 2015.
8.	Misaki Katsumoto, Michiyo Yamasaki, Yutaka Taketani, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : SNPs Associated with Serum Phosphorus Concentration in Japanese, American Society of Nephrology, kidney week 2014 Nov. 12-16, 2014 Philadelphia Convention Center, Philadelphia, PA, Nov. 2014.
9.	Abuduli Maerjianghan, Yutaka Taketani, Hirokazu Ohminami, Haruka Ueda and Eiji Takeda : Dietary Phosphate is a Novel Regulator of Glucose and Lipid Metabolism, American Society of Nephrology, kidney week 2014 Nov. 12-16, 2014 Philadelphia Convention Center, Philadelphia, PA, Nov. 2014.
10.	Hisami Okumura, K Sugihara, M Yamamoto, Yutaka Taketani, Tetsuya Ikemoto, Yusuke Arakawa, Satoru Imura, Yuji Morine, Satoru Imura, Mitsuo Shimada and Eiji Takeda : Recovery of non-protein respiratory quotient and health related quality of life after living-donor liver transplantation, 36th European Congress for Nutrition and Metabolism, Sep. 2014.
11.	Hisami Okumura, Akiyoshi Hirayama, Syoko Wada, Daisuke Kajiura, Masashi Masuda, Eiji Takeda, Yutaka Taketani, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada, Masaru Tomita and Tomoyoshi Soga : Perioperative serum and urine metabolome analysis in patients with hepatocellular carcinoma, 37th European Congress for Nutrition and Metabolism, Lisbon, Portugal, 2015, September 5-8, Sep. 2014.
12.	Kohei Sugihara, Hisami Okumura, Arisa Teramoto, Momo Yamamoto, Yutaka Taketani, Yu Saitou, Yusuke Arakawa, Mitsuo Shimada and Eiji Takeda : The non-protein respiratory quotient as biomarker for the recover from hepatectomy in patients with hepatocellular carcinoma., 36th European Congress for Nutrition and Metabolism, Geneva, Switzerland 2014, September 6-9, Sep. 2014.
13.	Hisami Okumura, Kohei Sugihara, Momo Yamamoto, Yutaka Taketani, Tetsuya Ikemoto, Yuji Morine, Satoru Imura, Mitsuo Shimada and Eiji Takeda : Recovery of non-protein respiratory quotient and health related quality of life after living-donor liver transplantation., 36th European Congress for Nutrition and Metabolism, Geneva, Switzerland 2014, September 6-9, Sep. 2014.
14.	Hisami Okumura, Akiyoshi Hirayama, Ayaka Kamimura, Satomi Yamasaki, Kohei Sugihara, Yutaka Taketani, Tomoyoshi Soga, Masaru Tomita and Eiji Takeda : Metabolome analysis after hyper- and hypoglycemic food intake in healthy young men, Tsuruoka, Yamagata, Japan, Jun. 2014.
15.	Hironori Yamamoto, Mina Kozai, Tomohiro Kagawa, Otoki Nakahashi, Shoko Ikeda, Rina Onishi, Yutaka Taketani and Eiji Takeda : Thyroid Hormones Decrease Plasma 1,25-Dihydroxyvitamin D Levels through Transcriptional Repression of the Renal 25-Hydroxyvitamin D3 1-Hydroxylase Gene (CYP27B1), American Society of Nephrology Kidney Week 2013, Atlanta, USA, Nov. 2013.
16.	Haruka Ueda, Yutaka Taketani, Maerjianghan Abuduli, Hirokazu Ohminami, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Lanthanum Carbonate or Dietary P Restriction Ameliorates Endothelial Dysfunction in Adenine-Induced Chronic Kidney Disease Rats, American Society of Nephrology Kidney Week 2014, Atlanta, USA, Nov. 2013.
17.	Michiyo Yamasaki, Misaki Katsumoto, Yutaka Taketani, Hisami Okumura and Eiji Takeda : Effects of Dietary Phosphorus Load on the Postprandial Blood Glucose and Glucose-Regulating Hormone Levels., American Society of Nephrology Kidney Week 2014, Atlanta, USA, Nov. 2013.
18.	Hisami Okumura, Akiyoshi Hirayama, Ayaka Kamimura, Satomi Yamasaki, Moe Takase, Kohei Sugihara, Chisaki Adachi, Yuka Kawakami, Tomoyoshi Soga, Masaru Tomita and Eiji Takeda : Low-rice intake in low energy density diet stimulates sweetness desire in women more than in Men, 9th Metabolomics Society 2013 Conference SECC, Glasgow, UK, Jul. 2013.
19.	Wanjihia W Violet, Ohminami Hirokazu, Yutaka Taketani, Kikuko Amou, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Gestational Isocaloric High Fat High Sucrose Diet Causes More Severe Metabolic Complications in Offspring than Calorie Restriction., American Diabetes Association Scientific Session 2013, Chicago, IL, USA, Jun. 2013.
20.	Kohei Sugihara, Hisami Okumura, Arisa Teramoto, Eri Urano, Takafumi Katayama, Hiroki Mori, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Recovery Pattern of Energy Metabolism and Blood Biochemical Data after Liver Resection in Hepatocellular Carcinoma Patients and Liver Transplantation Donors., 8th Asia Pacific Conference on Clinical Nutrition, Chiba, Japan, Jun. 2013.
21.	Violet Wanjihia, Hirokazu Ohminami, Yutaka Taketani, Kikuko Amou, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Metabolic programming of the steroyl-CoA desaturase 1 (SCD-1) gene after gestational isocaloric high fat high sucrose diet., 8th Asia-Pacific conference on Clinical Nutrition, Tokyo, June 9-12, 2013, Jun. 2013.
22.	Maerjianghan Abuduli, Yutaka Taketani, Hirokazu Ohminami, Haruka Ueda, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Effect of dietary phosphate-loading on glucose and lipid metabolism., 8th Asia-Pacific Conference on Clinical Nutrition, Tokyo, Japan, June 9-12, 2013, Jun. 2013.
23.	Yutaka Taketani, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Health effect of phosphorus: cardiovascular disease and mortality., 8th Asia-Pacific Conference on Clinical Nutrition, Tokyo, Japan, Jun. 2013.
24.	森本優香, 佐久間理英, 太田紘之, 梅田見名子, 石川真, Yutaka Taketani, Eiji Takeda and Hidekazu Arai : 24時間蓄尿を用いたリン摂取量の把握と妥当性の検討, 第16回日本病態栄養学会年次学術集会，京都，2013年1月12日~13日, Jan. 2013.
25.	Hironori Yamamoto, Nakao Mari, Nakahashi Otoki, Ikeda Shoko, Yutaka Taketani and Eiji Takeda : The Expression Profiling of Intestinal Nutrient Transporter and Channel Genes in Ratas with Renal Failure., Journal of the American Society of Nephrology, Vol.23, 951A, Oct. 2012.
26.	Nakao Mari, Hironori Yamamoto, Nakahashi Otoki, Kozai Mina, Yutaka Taketani and Eiji Takeda : Dietary Phosphate Restriction Prevents Renal Anemia in Chronic Kidney Disease Model Rats., Journal of the American Society of Nephrology, Vol.23, 792A, Oct. 2012.
27.	C Adachi, Hisami Okumura, B Zhou, Y Kawakami, Takafumi Katayama and Eiji Takeda : Effect of dietary energy density on fullness and satisfaction is modulated by habitual daily vegetable intake, 34th ESPEN Congress, Sep. 2012.
28.	A Teramoto, Hisami Okumura, Takafumi Katayama, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Comparison of measured REE with predicted BEE in Japanese cirrhosis, 34th ESPEN Congress, Barcelona, Sep. 2012.
29.	Hisami Okumura, A Teramoto, Takafumi Katayama, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Blood index for estimating non-protein respiratory quotient without using indirect calorimetry in cirrhotic patients, 34th ESPEN Congress, Barcelona, Sep. 2012.
30.	Hironori Yamamoto, Otani Ayako, Yokoyama Nozomi, Onishi Rina, Takei Yuichiro, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Regional Up-regulation of 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1) Gene Is Associated with the Pathogenesis of Ectopic Calcification in the Alpha Klotho Mutant Mice, 2012 Annual Meeting of the American Society for Bone and Mineral Research, Sep. 2012.
31.	Ikeda Shoko, Hironori Yamamoto, Nakahashi Otoki, Kozai Mina, Yutaka Taketani and Eiji Takeda : Induction of the Intact and C-terminal FGF23 Levels and Its Gene Expression in Lipopolysaccharide-Induced Acute Inflammation, 2012 Annual Meeting of the American Society for Bone and Mineral Research, Sep. 2012.
32.	Nakahashi Otoki, Hironori Yamamoto, Tanaka Sarasa, Kozai Mina, Yutaka Taketani, Ken-ichi Miyamoto, Kato Shigeaki and Eiji Takeda : Dietary Phosphorus Restriction Up-regulates the Ileal Fibroblast Growth Factor 15 Gene Expression through the Vitamin D Receptor Activation, 2012 Annual Meeting of the American Society for Bone and Mineral Research, Sep. 2012.
33.	B Zhou, Hisami Okumura, C Adachi, Y Kawakami, Takafumi Katayama and Eiji Takeda : Low-rice intake in low energy density diet stimulates sweetness desire in women more than in Men, American Diabetes Association 72rd Scientific Sessions, Chicago, IL, USA, Jun. 2012.
34.	Hironori Yamamoto, Kikuchi Hiroko, Nakao Mari, Nakahashi Otoki, Tanaka Sarasa, Yutaka Taketani and Eiji Takeda : THE EXPRESSION PROFILING OF INTESTINAL NUTRIENT TRANSPORTER GENES IN RATS WITH RENAL FAILURE, XVI International Congress on Nutrition and Metabolism in Renal Disease, Jun. 2012.
35.	Yutaka Taketani, Yamasaki Michiyo, Ueda Haruka, Mori Yukari, Tanaka Terumi, Horie Daisuke, Ominami Hirokazu, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : INTERACTION BETWEEN DIETARY PHOSPHATE AND CARBOHYDRATE ON GLUCOSE AND PHOSPHATE METABOLISMS IN HEALTHY YOUNG MEN., XVI International Congress on Nutrition and Metabolism in Renal Disease, Jun. 2012.
36.	Hironori Yamamoto, Masashi Masuda, Mina Kozai, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Regulation of Phosphate Homeostasis by Steroid/thyroid Hormones and Its Receptors, The International Conference on Food Factors 2011 (ICoFF 2011), Taipei, Taiwan, Nov. 2011.
37.	Rie Mukai, Tomoyuki Kawamura, Hisao Nemoto, Takeshi Nikawa, Hironori Yamamoto, Eiji Takeda and Junji Terao : Flavonoid derivatives prevent disuse muscle atrophy, Internatinal Conference on Food Factors, Taipei, Nov. 2011.
38.	Yutaka Taketani, Tan Vu Van, Eriko Watari, Tomoyo Kitamura, Abudli Maerujianghan, Terumi Tanaka, Hironori Yamamoto and Eiji Takeda : Hyperphosphatemia Causes Endothelial Dysfunction by Inhibiting Akt-Endothelial Nitric Oxide Synthase Pathway in Chronic Kidney Disease Rats, American Heart Association Scientific Sessions 2011, Orlando, FL, USA, Nov. 2011.
39.	Mina Kozai, Hironori Yamamoto, Ayako Otani, Shoko Ikeda, Otoki Nakahashi, Yutaka Taketani and Eiji Takeda : hyroid Hormones Decrease the Plasma 1alpha, 25-dihydroxyvitamin D3 Levels through Transcriptional Repression of the Renal 25-hydroxyvitamin D3 1alpha-hydroxylase (CYP27B1) Gene, American Society of Nephrology, Kidney Week 2011, Philadelphia, PA, USA, Nov. 2011.
40.	Yutaka Taketani, Tomoyo Kitamura, Hironori Yamamoto and Eiji Takeda : Elevated Extracellular Phosphate Levels Down-Regulate Both Akt and AMP-Dependent Kinase in Endothelial Cells, American Society of Nephrology, Kidney Week 2011, Philadelphia, PA, USA, Nov. 2011.
41.	Hironori Yamamoto, Tsuji Mitsuyoshi, Rie Mukai, T Inakuma, Junji Terao and Eiji Takeda : Dietary quercetin and onion powder could prevent immobilization induced bone loss in rats, 5th International Conference on Polyphenols and Health (ICPH), Barcelona, Oct. 2011.
42.	Tan Vu Van, Yutaka Taketani, Eriko Watari, Tomoyo Kitamura, Ken-ichi Miyamoto, Hironori Yamamoto and Eiji Takeda : ole of Akt-eNOS Signal Pathway in the Endothelial Dysfunction induced by Chronic Kidney Disease with Hyperphosphatemia., American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011.
43.	Shoko Ikeda, Hironori Yamamoto, Mina Kozai, Masashi Masuda, Sarasa Tanaka, Otoki Nakahashi, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Regulation of Renal Sodium-Dependent Phosphate Co-Transporters During Lipopolysaccharide-Induced Acute Inflammation., American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011.
44.	Hironori Yamamoto, Masashi Masuda, Mina Kozai, Sarasa Tanaka, Otoki Nakahashi, Shoko Ikeda, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : All-Trans-Retinoic Acid Inhibits Intestinal Phosphate Uptake and Type IIb Sodium-Dependent Phosphate Co-Transporter Gene Expression in Rat., American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011.
45.	Hisami Okumura, Akiko Taniguchi-Fukatsu, Yuka Kawakami, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : NATTO AND VISCOUS VEGETABLES IN A JAPANESE STYLE BREAKFAST IMPROVED INSULIN SENSITIVITY, LIPID METABOLISM AND OXIDATIVE STRESS IN IMPAIRED GLUCOSE TOLERANCE SUBJECTS, 33rd ESPEN Congress on Clinical Nutrition & Metabolism, Göteborg, Sweden, Sep. 2011.
46.	Eiji Takeda, Akiko Taniguchi-Fukatsu, Yuko Naniwa-Kuroki, Yuka Nishida, Hironori Yamamoto, Yutaka Taketani and Hisami Okumura : Natto And Viscous Vegetables Improved Insulin Sensitivity, Lipid Metabolism and Oxidative Stress in Impaired Glucose Tolerance Subjects, 7th Asia Pacific Conference of Clinical Nutrition, Bangkok, Thailand, Jun. 2011.
47.	Rie Mukai, Takeshi Nikawa, Hisao Nemoto, Hironori Yamamoto, Eiji Takeda, Yoshichika Kawai and Junji Terao : Disuse muscle atrophy is suppressed by antioxidative flavonoid quercetin, International Symposium on Free Radical Research: Contribution to Medicine, Kyoto, Jan. 2011.
48.	Rie Mukai, Tomoyuki Kawamura, Yutaka Fujikura, Moemi Hayashi, Hisao Nemoto, Takeshi Nikawa, Hironori Yamamoto, Eiji Takeda and Junji Terao : Disuse muscle atrophy is prevented by flavonoids, 2010 International Chemical Congress of Pacific Basin Societies, Honolulu, Dec. 2010.
49.	Rie Murai, Tomoyuki Kawamura, Yutaka Fujikura, Moemi Hayashi, Hisao Nemoto, Takeshi Nikawa, Hironori Yamamoto, Eiji Takeda and Junji Terao : Diused muscel atrophy is prevented by flavonoids, Pachifichem 2010, Honolulu, Dec. 2010.
50.	Ayako Otani, Hironori Yamamoto, Yuichiro Takei, Mina Kozai, Masashi Masuda, Shoko Ikeda, Otoki Nakahashi, Yutaka Taketani and Eiji Takeda : Regional Up-Regulation of 25-Hydroxyvitamin D 1a-Hydroxylase (CYP27B1) Gene Is Associated with the Pathogenesis of Ectopic Calcification in the alpha Klotho Mutant Mice, American Society of Nephrology Renal Week 2010, Denver, Colorado, USA, November 16-21, 2010, Nov. 2010.
51.	Masashi Masuda, Hironori Yamamoto, Mina Kozai, Yuichiro Takei, Otoki Nakahashi, Shoko Ikeda, Ayako Otani, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : All-Trans Retinoic Acid Maintains the Blood Phosphate Levels through the Positive and Negative Regulation of Type II Sodium-Dependent Phosphate Co-Transporter Family Genes in Kidney and Intestine, American Society of Nephrology Renal Week 2010, Denver, Colorado, USA, November 16-21, 2010, Nov. 2010.
52.	Tan Vu Van, Eriko Watari, Yutaka Taketani, Tomoyo Kitamura, Asuka Shiota, Ayako Tanimura, Hironori Yamamoto and Eiji Takeda : Dietary Phosphate Restriction Ameliorates Endothelial Function in Adenine-Induced Chronic Kidney Disease Model Rats, American Society of Nephrology Renal Week 2010, Denver, Cololado, USA, November 16-21, 2010, Nov. 2010.
53.	Tomoyo Kitamura, Yutaka Taketani, Eriko Watari, Asuka Shiota, Tan Vu Van, Terumi Tanaka, Hironori Yamamoto and Eiji Takeda : Phosphoproteomic Analysis in the Endothelial Cells Damaged by Hyperphosphatemia, American Heart Association Scientific Session 2010, Chicago, IL, USA, November 13-17, 2010, Nov. 2010.
54.	Yuichiro Takei, Hironori Yamamoto, Tadashi Sato, Masashi Masuda, Ayako Otani, Yutaka Taketani, Beate Lanske and Eiji Takeda : Up-regulation of Stanniocalcin 2 Expression by the Abnormality of Klotho-Fgf23 Signaling and Inhibition of Phosphate-induced Calcification in Aortic Vascular Smooth Muscle Cells, American Society for Bone and Mineral Research 2010 Annual Meeting, Toronto, ON, Canada, October 15-19, 2010, Oct. 2010.
55.	Mina Kozai, Hironori Yamamoto, Masashi Masuda, Yuichiro Takei, Sarasa Tanaka, Yutaka Taketani, Ken-ichi Miyamoto, Shigeaki Kato and Eiji Takeda : Transrepression of Renal 25-hydroxyvitamin D3 1-hydroxylase (CYP27B1) Gene Expression by Thyroid Hormone Receptor 1, American Society for Bone and Mineral Research 2010 Annual Meeting, Toronto, Canada, October 15-19, 2010, Oct. 2010.
56.	Yuka Kawakami, Hisami Okumura, Masae Sakuma, Yukie Matsumoto, Tadatoshi Sato and Eiji Takeda : Gene expression profiling of human peripheral blood is affected by the differences in glycemic and insulinemic responses to food intake, 32th ESPEN congress, Nice, France, Sep. 2010.
57.	Hisami Okumura, Rika Yamauchi, Eri Urano, Takafumi Katayama, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : Identification of laboratory biomarker reflecting non protein respiratory quotient (npRQ) in hepatic cirrhosis, 32th ESPEN congress, Nice, France, Sep. 2010.
58.	Hisami Okumura, Akiko Taniguchi-Fukatsu, Yuka Kawakami, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : Effect of viscous mixed meal on glucose lipid metabolism and oxidant stress, 33th ESPEN congress, Gothenburg, Sweden, Sep. 2010.
59.	Hirokazu Ominami, Kikuko Amou, Yutaka Taketani, Takashi Uebanso, Kazusa Sato, Makiko Fukaya, Hidekazu Arai, Megumi Koganei, Hajime Sasaki, Hironori Yamamoto and Eiji Takeda : Combined Efects of Dietary Carbohydrate and Fat on Tissue Fatty Acid Composition and Insulin Resistance, American Diebetes Association 70th Scientific Sessions 2010, Orlando, FL, USA, June 25-29, 2010, Jun. 2010.
60.	Takashi Uebanso, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, Hidekazu Arai, Yuichiro Takei, Masashi Masuda, Ayako Tanimura, Hisami Okumura and Eiji Takeda : Human FGF21 Is Paradoxically Induced by Both Fasting and Over-Feeding Signals - Is FGF21 a Nutritional Adaptation Factor?, American Diebetes Association 70th Scientific Sessions 2010, Orlando, FL, USA, June 25-29, 2010, Jun. 2010.
61.	Kikuko Amou, Hirokazu Ominami, Yutaka Taketani, Kazusa Sato, Makiko Fukaya, Takashi Uebanso, Hidekazu Arai, Megumi Koganei, Hajime Sasaki, Hironori Yamamoto and Eiji Takeda : The Interaction of Dietary Carbohydrate and Fat on Pancreatic Islet Dysfunction Mediated by Glucolipotoxicity, American Diebetes Association 70th Scientific Sessions 2010, Orlando, FL, USA, June 25-29, 2010, Jun. 2010.
62.	Emi Shuto, Yutaka Taketani, W Kusunise, T Tanaka, D Horie, Kikuko Amou, Hironori Yamamoto, Tohru Sakai and Eiji Takeda : Excessive dietary phosphorus acutely impairs endothelial function in healthy men, The American Society of Nephrology 42nd ANNUAL MEETING & Scientific Exposition, San Diego, Oct. 2009.
63.	Emi Shuto, Yutaka Taketani, R Tanaka, Ayako Tanimura, T Uebanso, M Isshiki, Nagakatsu Harada, Hironori Yamamoto, Yutaka Nakaya and Eiji Takeda : Postprandial Hyperphosphatemia is a Novel Risk Factor for Cardiovascular Disease by Involving Endothelial Dysfunction, American Society of Bone and Mineral Research 30th ANNUAL MEETING, Montreal, Sep. 2008.
64.	Hisami Okumura, Akiko Taniguchi, Yuko Naniwa, Yasuko Takahashi and Eiji Takeda : Effect of viscous mixed meal on glucose lipid metabolism and oxidant stress, 32th ESPEN congress, Nice, France, 15th International Congress of Dietetics Yokohama, Sep. 2008.
65.	Emi Shuto, Yutaka Taketani, R Tanaka, Ayako Tanimura, M Isshiki, Nagakatsu Harada, Hironori Yamamoto and Eiji Takeda : Hyperphosphatemia mediates oxidative stress in bovine aortic endothelial cells, American Society of Bone and Mineral Research 29th ANNUAL MEETING, Honolulu, Sep. 2007.
66.	Eiji Takeda : Metabolic control by low glycemic index diet and gene expression, ILSI's First International Conference on NUTRIGENOMICS Opportunities in Asia, Singapore, Dec. 2005.
67.	Eiji Takeda, Yutaka Taketani, K. Nashiki, E. Shuto and Hironori Yamamoto : PHOSPHATE-MEDIATED INTRACELLULAR SIGNAL TRANSDUCTION PATHWAYS AND IT'S FUNCTION, Forty-Sixth International Symposium on `Regulation of Enzyme Activity and Synthesis in Normal and Neoplastic Tissues`, Bologna, Oct. 2005.
68.	M. Tsuji, Hisami Okumura, Yutaka Taketani, T. Sato, K. Nashiki, Hironori Yamamoto and Eiji Takeda : Postprandial changes of serum fibroblast growth factor23(FGF23) levels on high phosphate diet in healthy men, 27th Annual Meeting of American Society for Bone and Mineral Research, Tennessee, USA, Sep. 2005.
69.	Yutaka Taketani, K. Nashiki, A. Nakamura, N. Sawada, Hironori Yamamoto, Hidekazu Arai and Eiji Takeda : Role of ezrin in the parathyroid hormone-mediated downregulation of so dium-dependent phosphate transporter(NaPi-IIa) in opossum kidney cells, 27th Annual Meeting of American Society for Bone and Mineral Research, Tennessee, USA, Sep. 2005.
70.	Eiji Takeda, Hidekazu Arai, M. Sakuma, Yutaka Taketani, Akira Mizuno, T. Doi, M. Koganei and H. Sasaki : Effects of palatinose-based liquid diet (Inslow) intake on substrate oxidation and second meal effect in healthy men, 27th ESPEN Congress, Brussels, Belgium, Aug. 2005.
71.	Hironori Yamamoto, Yutaka Taketani, M. Tsuji, T. Sato, Hidekazu Arai and Eiji Takeda : A novel splicing variant transcript of the renal type a sodium-dependent phosphate cotransporter (NPT2a) gene is positively and negatively regulated by 1,25-dihydroxyvitamin D3 and phex cleavable humoral factors, 26th Annual Meeting of American Society for Bone and Mineral Research, Seattle, Oct. 2004.
72.	Yutaka Taketani, T. Takeichi, K. Nashiki, Hironori Yamamoto, N. Sawada, M. Ichikawa, Hidekazu Arai and Eiji Takeda : PTH-stimulated signaling molecules that are involved in the endpcytosis of NaPi-IIa phosphate transporter are compartmentalized and activated in caveolae-like micro domains, 26th Annual Meeting of American Society for Bone and Mineral Research, Seattle, Oct. 2004.
73.	Hiroki Moriguchi, Tomiaki Morikawa, Hideki Nakanishi, Kazuya Matsumoto, Eiji Takeda and Takafumi Katayama : Clinical support system with WBT for pressure ulcer care, E-learn 2004, Phoenix,USA, 2004.
74.	Eiji Takeda : Regulation and Function of Phosphate in the Body, The 3rd International Conference on Food Factors: Physiologic Functions and Disease Risk Reduction, Tokyo, Dec. 2003.
75.	Eiji Takeda : Nutirition Guidance for Osteoporosis Based on Types of Vitamin D Receptor Gene Polymorphism, The 4th International Conference on Nutrition and Aging, Tokyo, Nov. 2003.
76.	T. Sato, Kyoko Morita, Y. Kado, Hironori Yamamoto, Yutaka Taketani, Y. Nii and Eiji Takeda : Decreased Vitamin D-Dependent Intestinal Calcium Absorption in Immobilized Rats, 25th Annual Meeting of American Society for Bone and Mineral Research, Mineneapolis,Minnesota, USA, Sep. 2003.
77.	Yutaka Taketani, K. Nashiki, N. Sawada, Hironori Yamamoto, M. Ichikawa, Kyoko Morita, Hidekazu Arai and Eiji Takeda : Subcellular Localizayion and PTH-Dependent Translocation of NaPi-IIa in Renal Proximal Tubular Cells, 25th Annual Meeting of American Society for Bone and Mineral Research, Mineneapolis,Minnesota, USA, Sep. 2003.
78.	Yutaka Taketani, N. Amizuka, C. Ogawa, N. Sawada, K. Nomoto, Hidekazu Arai and Eiji Takeda : CAVEOLIN IN THE MATRIX VESICLES RELEASED FROM OSTEOBLAST, 2003年国際骨代謝学会・日本骨代謝学会第1回合同国際会議, Osaka, Jun. 2003.
79.	Yutaka Taketani, M Nomoto, Hironori Yamamoto, Kyoko Morita, M Isshiki, S Kato and Eiji Takeda : Induction of 25-hydroxyvitamin D-1alpha-hydroxylase mRNA by phosphate depletion, 24th Annual Meeting of American Society for Bone and Mineral Research, San Antonio, Texas, USA, Sep. 2002.
80.	Eiji Takeda, Hidekazu Arai, Hironori Yamamoto, M. Kubota, S. Yoshida, Zhang Honghong, Yutaka Taketani, Kyoko Morita and Ken-ichi Miyamoto : Human vitamin D receptor gene Expression in intestine and osteoporosis, The 2nd China-Japan International Conference on Vitamins, Shanghai, Oct. 2001.
81.	Eiji Takeda : The polymorphism in the candal-related homedomain protein CDX-2 binding element in the human vitamin D receptor gene., The 2nd China-Japan International Conference on Vitamins, Shanghai, Oct. 2001.
82.	M. Iida, Kyoko Morita, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Internalization pathway of renal phosphate transporter mediated chloride channel, 23rd Annual Meeting of American Society for Bone and Mineral Research, Phoenix,Arizona, Oct. 2001.
83.	Hironori Yamamoto, K. Kobayashi, Y. Tani, Yutaka Taketani, Kyoko Morita, Hidekazu Arai, Ken-ichi Miyamoto, S. Kato, J. Pike and Eiji Takeda : Renal cell-specific regulation of type IIa sodium-dependent phosphate cotranspoter gene expression by 1, 25-dihydroxyvitamin D3, 23rd Annual Meeting of American Society for Bone and Mineral Research, Phoenix,Arizona, Oct. 2001.
84.	Hisami Yamanaka, H. Miyake, S. Tashiro and Eiji Takeda : Effect of late evening snack on energy metabolism in liver cirrhosis, 17th International Congress of Nutrition, Vinna,Austria, Aug. 2001.
85.	Kyoko Morita, M. Iida, Yutaka Taketani and Eiji Takeda : Effect of soybean isoflavone on bone metabolism, 17th International Congress of Nutrition, Vinna,Austria, Aug. 2001.

Proceeding of Domestic Conference:

1.	池田翔子, Hironori Yamamoto, 増田真志, 中橋乙起, 橋本脩平, 向原理恵, 中尾真理, Yutaka Taketani and Eiji Takeda : 敗血症時におけるリン代謝異常の分子メカニズムの解析, 第14回日本病態栄養学会年次学術集会,
2.	上番増喬, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, 田中更沙, Hidekazu Arai, 大南博和, Hisami Okumura and Eiji Takeda : コレステロール摂取はFGF21mRNA発現を抑制する, 第13回日本病態栄養学会年次学術集会,
3.	大南博和, Kikuko Amou, Yutaka Taketani, 上番増喬, 佐藤佳瑞智, 深谷牧子, Hidekazu Arai, 小金井恵, 佐々木一, Hironori Yamamoto and Eiji Takeda : 組織の脂肪酸組成に対して食餌性糖・脂質の組合せが与える影響とインスリン抵抗性への関連性, 第53回日本糖尿病学会学術集会,
4.	Eiji Takeda : 栄養管理法について, 四国NMCクラブ講演,
5.	Masashi Masuda, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : All-transレチノイン酸による小腸ナトリウム依存性リン酸トランスポーター遺伝子発現抑制機構, 第366回脂溶性ビタミン総合研究委員会プログラム, Dec. 2020.
6.	Hironori Yamamoto, 田尻真梨, 中橋乙起, Masashi Masuda, Hirokazu Ohminami, Kohta Ohnishi, 石黒真理子, 池田涼子, 岩野正之, Eiji Takeda and Yutaka Taketani : 糖尿病時におけるビタミンD・カルシウム代謝異常の分子機構の解明, 第67回日本栄養改善学会学術集会, Sep. 2020.
7.	Hironori Yamamoto, Mari Tajiri, Otoki Nakahashi, Masashi Masuda, Hirokazu Ohminami, Kohta Ohnishi, Eiji Takeda and Yutaka Taketani : 糖尿病時におけるビタミンD・カルシウム代謝異常の分子機構の解明, The 74th Annual Meeting of Japan Society of Nutrition and Food Science, Apr. 2020. (Keyword) vitamin D / calcium / diabetes
8.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, Eiji Takeda, 佐藤美智子, 隅田奈美, 久米寛子, 大前博司, 森下照大, 川浦昭彦, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue and Yutaka Taketani : 骨格筋肉量，機能，栄養素吸収におよぼす1日1000IUのビタミンD摂取効果, Vitamins, Vol.94, No.4, 277, Apr. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Hydroxycholecalciferols(血液) Vitamin D(薬理学) 筋骨格系生理学的現象乳骨格筋身体組成生理的吸収筋量ヒト成人(19~44) 中年(45~64) 高齢者(65~79) 男女
9.	Tomohiro Kagawa, Hironori Yamamoto, Otoki Nakahashi, Nagakatsu Harada, Masashi Masuda, Eiji Takeda and Yutaka Taketani : ステロール調節エレメント結合蛋白質SREBPはビタミンD代謝酵素CYP24A1の発現を調節する, 第73回日本栄養・食糧学会大会, May 2019.
10.	Sachi Nii, Misaki Katsumoto, Yoko Narasaki, Chihiro Seko, Michiyo Yamasaki, Hisami Okumura, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : 一塩基多型rs1697421は食後血清リンに影響する, 第22回日本臨床内分泌病理学会学術集会(徳島大学大塚講堂), Sep. 2018.
11.	Hironori Yamamoto, 香川知博, 中橋乙起, 石黒真理子, Masashi Masuda, Eiji Takeda and Yutaka Taketani : 生体ビタミンD代謝の日内リズムの制御機構の解明, 日本ビタミン学会第69回大会, Jun. 2017.
12.	Hironori Yamamoto, 香川知博, 中橋乙起, 石黒真理子, Masashi Masuda and Eiji Takeda : 生体ビタミンD代謝の日内リズムの制御機構の解明, 第71回日本栄養・食糧学会大会, May 2017.
13.	杉原康平, Masashi Masuda, 中尾真理, Abuduli Maerjianghan, 石田陽子, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : リンの過剰摂取はDSS誘発性大腸炎を悪化させる, 第19回日本病態栄養学会年次学術集会，パシフィコ横浜，神奈川県横浜市，2016年1月9日~10日, Jan. 2016.
14.	Abuduli Maerjianghan, 大南博和, Hiroshi Sakaue, Tamaki Otani, 上田遥香, Eiji Takeda and Yutaka Taketani : 食事性のリンが糖代謝に及ぼす影響:PET/CT用いた解析, 第36回日本肥満学会，名古屋国際会議場，愛知県名古屋市，2015年10月2日~3日, Oct. 2015.
15.	中尾真理, Hironori Yamamoto, 福田詩織, Yutaka Taketani and Eiji Takeda : 食餌性リンによる鉄欠乏性貧血の進展及び鉄代謝に及ぼす影響, 第33回日本骨代謝学会学術集会，京王プラザホテル，東京都新宿区，2015年7月23日~25日, Jul. 2015.
16.	福田詩織, Hironori Yamamoto, 中尾真理, Eiji Takeda and Yutaka Taketani : 食餌性リンによる腎αーklotho発現制御と異所性石灰化の発症, 第33回日本骨代謝学会学術集会，京王プラザホテル，東京都新宿区，2015年7月23日~25日, Jul. 2015.
17.	Hironori Yamamoto, 池田翔子, 糸魚川玲子, 加藤愛理, 小寺里奈, 源甲斐優美, 石黒真理子, Yutaka Taketani and Eiji Takeda : 急性炎症時における生体ビタミンD代謝変動の解析, 日本ビタミン学会第67回大会，奈良県新公会堂，奈良県奈良市，2015年6月5日~6日, Jun. 2015.
18.	中尾真理, Hironori Yamamoto, 中橋乙起, 池田翔子, 阿部航太郎, 福田詩織, Eiji Takeda and Yutaka Taketani : 慢性腎不全モデルラットにおける鉄代謝異常と食餌性リンの影響, 日本ビタミン学会第67回大会，奈良県新公会堂，奈良県奈良市，2015年6月5日~6日, Jun. 2015.
19.	福田詩織, Hironori Yamamoto, 中橋乙起, 池田翔子, 中尾真理, 横山望, 吉川亮平, 大西里奈, Eiji Takeda and Yutaka Taketani : 成長期における食餌性リンによるalpha-klotho発現制御, 日本ビタミン学会第67回大会，奈良県新公会堂，奈良県奈良市，2015年6月5日~6日, Jun. 2015.
20.	和田宵湖, Hisami Okumura, Eiji Takeda, Yutaka Taketani, Takafumi Katayama, Yusuke Arakawa, Satoru Imura and Mitsuo Shimada : 肝癌患者における肝切除前後のエネルギー代謝変化の検討, 第2回日本栄養改善学会四国支部学術総会, Apr. 2015.
21.	和田宵湖, Hisami Okumura, 杉原康平, 山本モモ, Yutaka Taketani, Mitsuo Shimada and Eiji Takeda : 肝癌患者における切除量が切除前後のエネルギー代謝に及ぼす影響, 第18回日本病態栄養学会年次学術集会平成27年1月10-11日国立京都国際会館, Jan. 2015.
22.	多々納浩, Hisami Okumura, 周蓓, Takafumi Katayama, Yutaka Taketani and Eiji Takeda : 脂質摂取量の多い食習慣による食欲や嗜好性への影響についての検討, 第18回日本病態栄養学会年次学術集会平成27年1月10-11日国立京都国際会館, Jan. 2015.
23.	Yoko Narasaki, Yutaka Taketani, Sayaka Matsura, 森西真由美, 米田武志, 山崎通世, 勝本美咲, Yasuhiro Hamada and Eiji Takeda : 食品毎のリン負荷指数の確立, 第18回日本病態栄養学会年次学術集会平成27年1月10-11日国立京都国際会館, Jan. 2015.
24.	勝本美咲, Yutaka Taketani, 山崎通世, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : 日本人における血清リン濃度と関連するSNP, 第18回日本病態栄養学会年次学術集会平成27年1月10-11日国立京都国際会館, Jan. 2015.
25.	杉原康平, Hisami Okumura, 和田宵湖, 山本モモ, Yutaka Taketani, Shin-ichiro Yamada, Satoru Imura, Mitsuo Shimada and Eiji Takeda : 肝細胞癌患者における肝切除術後予後因子としての非蛋白質呼吸商, 第18回日本病態栄養学会年次学術集会平成27年1月10-11日国立京都国際会館, Jan. 2015.
26.	Eiji Takeda, Hisami Okumura, 和田宵湖, 山本もも, 杉原康平, Yuji Morine, Satoru Imura and Mitsuo Shimada : 中遊離脂肪酸(NEFA)濃度を指標とした就寝前夜食(LES)療法の適応, 第45回日本消化吸収学会総会, Nov. 2014.
27.	伊美友紀子, Yutaka Taketani, Maerjianghan Abuduli, 矢引紀江, 谷口由莉, 大南博和 and Eiji Takeda : リン過剰摂取による脂肪量減少の意義, 第35回日本肥満学会シーガイアコンベンションセンター，宮崎市平成26年10月24-25日, Oct. 2014.
28.	谷口由莉, Yutaka Taketani, 大南博和, Maerjianghan Abuduli, 伊美友紀子, Hiromi Sakata-Haga, Hironori Yamamoto and Eiji Takeda : 食餌性リンが摂食調節機構に及ぼす影響, 第35回日本肥満学会シーガイアコンベンションセンター，宮崎市平成26年10月24-25日, Oct. 2014.
29.	Hisami Okumura, 足立知咲, Akiko Matsumura, Yutaka Taketani and Eiji Takeda : 低エネルギー密度の日本食摂取後における男女の嗜好性に対する違いの検討, 第61回日本栄養改善学会学術総会平成26年8月20-22日パシフィコ横浜, Aug. 2014.
30.	Hironori Yamamoto, 大西里奈, 福田詩織, 竹井悠一郎, Yutaka Taketani and Eiji Takeda : FGF23/α-klothoシグナル異常による異所性石灰化発症とFetuin-Aの発現変動, 第32回日本骨代謝学会学術集会，平成26年7月24日—26日，大阪国際会議場, Jul. 2014.
31.	Sayaka Matsura, Yutaka Taketani, 森西真由美, 米田武志, 山崎通世, 勝本美咲, Yasuhiro Hamada and Eiji Takeda : 食品中リンの生体利用率の評価, 第57回日本腎臓学会, Jul. 2014.
32.	Sayaka Matsura, Yutaka Taketani, 森西真由美, 米田武志, 山崎通世, 勝本美咲, Yasuhiro Hamada and Eiji Takeda : 食品中リンの生体利用率の評価, 第57回日本腎臓学会学術総会平成26年7月4-6日パシフィコ横浜, Jun. 2014.
33.	Yutaka Taketani, 松浦明香, 森西真由美, 米田武志, 山崎通世, 勝本美咲, Yasuhiro Hamada and Eiji Takeda : 食品毎のリン生体利用率を利用したリン制限食の可能性, 第2回日本腎不全栄養研究会学術集会・総会平成26年6月29日新大阪ブリックビル, Jun. 2014.
34.	Yutaka Taketani, 森西真由美, 松浦明香, 米田武志, 山崎通世, 勝本美咲, Yasuhiro Hamada, Hisami Okumura and Eiji Takeda : 食品毎のリン生体利用率の違いを利用したリン制限食の可能性, 第2回日本腎不全栄養研究会, Jun. 2014.
35.	Hironori Yamamoto, 向原理恵, 中橋乙起, 香川知博, 藤本和輝, 中尾真理, 青木菜摘, 柴田重信, Yutaka Taketani and Eiji Takeda : ビタミンD代謝の日内リズムの分子機構の解明および時間治療への応用, 日本ビタミン学会第66回大会，平成26年6月13日，14日，姫路商工会議所, Jun. 2014.
36.	Shiori Fukuda, Hironori Yamamoto, Otoki Nakahashi, Shoko Ikeda, Nozomi Yokoyama, Ryohei Yoshikawa, Rina Ohnishi, Yutaka Taketani and Eiji Takeda : 食餌性リンによる腎α-kloyho発現制限と異所性石灰化の発症, 第68回日本栄養・食糧学会大会平成26年5月30日-6月1日札幌市教育文化会館，酪農学園大学, May 2014.
37.	Hiroshi Tatano, Hisami Okumura, Bei Zhou, Yutaka Taketani and Eiji Takeda : 油摂取の多い食習慣による嗜好への影響についての検討, 第1回日本栄養改善学会四国支部学術総会，平成26年5月17日，徳島大学大塚講堂小ホール, May 2014.
38.	多々納浩, Hisami Okumura, 周蓓, Yutaka Taketani and Eiji Takeda : 油摂取の多い食習慣による嗜好への影響についての検討, 第1回中四国栄養改善学会, May 2014.
39.	Mami Kanamoto, Yasuhiro Hamada, Yutaka Nakaya, Eiji Takeda, Hisami Okumura, Toru Utsunomiya, Satoru Imura, Yuji Morine, Tetsuya Ikemoto, Yusuke Arakawa, Hiroki Mori and Mitsuo Shimada : NST介入による周術期栄養管理の有用性に関する検討, 第114回日本外科学会定期学術集会, Apr. 2014.
40.	杉原康平, Hisami Okumura, Satoru Imura, Mitsuo Shimada, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : エネルギー代謝による生体肝移植後早期における栄養評価, 第17回日本病態栄養学会, Jan. 2014.
41.	山本モモ, Hisami Okumura, 杉原康平, 寺本有沙, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : 肝硬変患者における窒素出納評価の問題点についての検討, 第17回日本病態栄養学会, Jan. 2014.
42.	Hisami Okumura, 足立知咲, 周蓓, 関さやか, 多々納浩, 杉原康平, 山本もも, 山崎聡美, 藤岡真理子, 上村綾佳, 川上由香, 稲葉廣美, Takafumi Katayama and Eiji Takeda : エネルギー密度に注目した低エネルギーでも満腹度・満足度の高い食事ガイドラインの作成, 第17回日本病態栄養学会, Jan. 2014.
43.	Hisami Okumura, 平山明由, 上村綾佳, 山崎聡美, 高瀬萌子, 川上由香, 曽我朋義, 冨田勝 and Eiji Takeda : メタボローム解析を用いた高GIおよび低GI食品摂取後の血清代謝物への影響, 第17回日本病態栄養学会, Jan. 2014.
44.	Yoshiko Tani, Taiki Furumoto, Shizue Yamada, Sonoko Yasui, Akiko Uebanso, Shuhei Hashimoto, Chisaki Adachi, Noriko Nagao, Akiko Matsumura, Eiji Takeda, Yutaka Nakaya, Shinsuke Katoh and Yasuhiro Hamada : くも膜下出血患者における栄養管理がリハビリテーション及び合併症に及ぼす影響, 第17回日本病態栄養学会, Jan. 2014.
45.	杉原康平, Hisami Okumura, 山本モモ, 柏原秀也, Kouzou Yoshikawa, Toru Utsunomiya, Nobuhiro Kurita, Mitsuo Shimada and Eiji Takeda : スリーブ状胃切除術前後のエネルギー代謝評価, 第5会日本静脈経腸栄養学会四国支部会学術集会, Sep. 2013.
46.	杉原康平, Hisami Okumura, 寺本有沙, Eiji Takeda, Hiroki Mori, Toru Utsunomiya and Mitsuo Shimada : エネルギー代謝と血液生化学検査からみた肝切除術前後の栄養評価, 第247回徳島医学会, Aug. 2013.
47.	Yutaka Taketani, Hironori Yamamoto, Hisami Okumura and Eiji Takeda : CKD-MBDの管理における食事性リン, 第58回日本透析医学会学術集会・総会(ワークショップ)，福岡，6月20日~23日，2013年, Jun. 2013.
48.	吉川亮平, Hironori Yamamoto, 香川知博, 中橋乙起, 横山望, 大西里奈, 池田翔子, Yutaka Taketani and Eiji Takeda : マウス腎α-klotho発現に与える加齢および食事性リンの影響, 第67回日本栄養・食糧学会大会，名古屋，5月24日~26日，2013年, May 2013.
49.	中尾真理, Hironori Yamamoto, 阿部航太郎, 中橋乙起, 池田翔子, Yutaka Taketani and Eiji Takeda : リン補給は鉄欠乏性貧血の進展を予防する, 第67回日本栄養・食糧学会大会，名古屋，5月24日~26日，2013年, May 2013.
50.	Hironori Yamamoto, 香西美奈, 香川知博, Nagakatsu Harada, 中橋乙起, 池田翔子, Yutaka Taketani and Eiji Takeda : 甲状腺ホルモンは腎臓25水酸化ビタミンD3ー1α水酸化酵素遺伝子(CYP27B1)の転写抑制により血中活性型ビタミンD濃度を低下させる, 第67回日本栄養・食糧学会大会，名古屋，5月24日~26日，2013年, May 2013.
51.	香川知博, Hironori Yamamoto, 香西美奈, Nagakatsu Harada, 向原理恵, Yutaka Taketani and Eiji Takeda : ビタミンD3-24水酸化酵素CYP24A1の新たな発現調節因子の同定, 日本ビタミン学会第65回大会，東京，5月17日~18日，2013年, May 2013.
52.	Hironori Yamamoto, 田尻真梨, 中橋乙起, 香西美奈, 香川知博, Yutaka Taketani and Eiji Takeda : 糖尿病時におけるビタミンD・カルシウム代謝異常の分子機構の解明, 日本ビタミン学会第65回大会，東京，5月17日~18日，2013年, May 2013.
53.	Hironori Yamamoto, 香西美奈, 香川知博, Yutaka Taketani and Eiji Takeda : CKD, 第56回日本腎臓学会学術集会(ワークショップ)，東京，5月10日~12日，2013年, May 2013.
54.	佐藤千穂, 冨岡麗子, 山上真樹子, 宮本登志子, Munehide Matsuhisa, Hiroshi Kitahata, Eiji Takeda, Hiro-omi Kanayama, Hiroaki Yanagawa, 木下成三 and 川島周 : 徳島県内の医療機関における倫理審査体制に関する状況調査, 第246回徳島医学会学術集会, Feb. 2013.
55.	高瀬萌子, Hisami Okumura, 川上由香, 平山明由, 曽我朋義, 冨田勝 and Eiji Takeda : 健常者および肥満者に対する75gOGTT後のメタボローム解析プロファイル, 第16回日本病態栄養学会, Jan. 2013.
56.	寺本有沙, Hisami Okumura, 杉原康平, Takafumi Katayama, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : 肝癌および肝移植ドナーの肝切除術前後におけるエネルギー代謝の評価, 第16回日本病態栄養学会, Jan. 2013.
57.	杉原康平, Hisami Okumura, 寺本有沙, Hiroki Mori, Toru Utsunomiya, Mitsuo Shimada and Eiji Takeda : 肝癌および肝移植ドナーの肝切除術前後におけるエネルギー代謝の評価, 第16回日本病態栄養学会, Jan. 2013.
58.	周蓓, Hisami Okumura, 足立知咲, 川上由香, 稲葉廣美, 細川敦子, 森永良二, 片山隆文 and Eiji Takeda : エネルギーの異なる昼食摂取後の満腹度・満足度に対する年齢の影響, 第16回日本病態栄養学会, Jan. 2013.
59.	足立知咲, Hisami Okumura, 藤岡真理子, 山崎聡美, 高瀬萌子, 杉原康平, 寺本有沙 and Eiji Takeda : エネルギー密度に着目した低エネルギーで満腹度・満足度の高い食事献立の検討, 第16回日本病態栄養学会, Jan. 2013.
60.	Hisami Okumura, 足立知咲, 周蓓, 川上由香, 稲葉廣美, 細川敦子, 森永良二, 片山貴文 and Eiji Takeda : エネルギー密度を指標とした低エネルギーで満腹度・満足度の高い昼食の検討, 第16回日本病態栄養学会, Jan. 2013.
61.	田尻真梨, Hironori Yamamoto, 中橋乙起, 香川知博, Yutaka Taketani, 佐々木一 and Eiji Takeda : 糖尿病時におけるビタミンD代謝異常の解明とリン制限食の治療効果, 第16回日本病態栄養学会年次学術集会，京都，2013年1月12日~13日, Jan. 2013.
62.	Rumi Katashima, 佐藤千穂, 冨岡麗子, 山上真樹子, 宮本登志子, 木下成三, 川島周, Munehide Matsuhisa, Hiroshi Kitahata, Eiji Takeda, Hiro-omi Kanayama and Hiroaki Yanagawa : 徳島県内の医療機関における倫理審査体制に関する状況調査, 第33回日本臨床薬理学会年会, Nov. 2012.
63.	Maerjianghan Abduli, Yutaka Taketani, 大南博和, 上田遙香, 谷口由莉, Hironori Yamamoto and Eiji Takeda : 長期的高リン食摂取が糖代謝および脂質代謝に及ぼす影響(会議録), Journal of Japan Society for the Study of Obesity, Vol.18, No.Supplement, 175, Sep. 2012.
64.	Eiji Takeda, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : オーダーメイド栄養学オーダーメイド臨床栄養管理, New Diet Therapy, Vol.28, No.2, 109, Sep. 2012.
65.	Hironori Yamamoto, 向原理恵, 中橋乙起, 池田翔子, 香西美奈, Yutaka Taketani and Eiji Takeda : 生体リン・ビタミンD代謝の概日リズムの分子機構の解明, 第30回日本骨代謝学会学術集会プログラム抄録集, 193, Jul. 2012.
66.	Hironori Yamamoto, 大谷彩子, 横山望, 香西美奈, 池田翔子, Yutaka Taketani and Eiji Takeda : α Klotho-Fgf23シグナル異常による25-ヒドロキシビタミンD3-1α水酸化酵素(CYP27B1)発現亢進と異所性石灰化発症の分子機構の解明, 第30回日本骨代謝学会学術集会プログラム抄録集, 233, Jul. 2012.
67.	Eiji Takeda, Hironori Yamamoto, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, Yutaka Taketani, Tatsuya Tominaga and Toshio Doi : 1.局所的CYP27B1発現亢進による異所性石灰化(第334回会議研究発表要旨,脂溶性ビタミン総合研究委員会), Vitamins, Vol.86, No.5, 358-359, Jun. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680677126528 (CiNii: 1390282680677126528)
68.	Eiji Takeda, Hironori Yamamoto, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, Yutaka Taketani, Tatsuya Tominaga and Toshio Doi : 局所的CYP27B1発現亢進による異所性石灰化, Vitamins, Vol.86, No.5-6, 358-359, Jun. 2012.
69.	向原理恵, Hironori Yamamoto, 中橋乙起, 池田翔子, 香西美奈, Yutaka Taketani and Eiji Takeda : 1-III-11 リン・ビタミンD代謝の概日リズムの解析(一般演題要旨,日本ビタミン学会第64回大会講演要旨), Vitamins, Vol.86, No.4, 244, Apr. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680761309824 (CiNii: 1390282680761309824)
70.	上田遙香, アブドリマルジャンハン, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : CKDモデルラットにおける血管内皮機能障害に対する炭酸ランタンの効果(会議録), Japanese Journal of Nephrology, Vol.54, No.3, 321, Apr. 2012.
71.	大南博和, Wanjihia Violet, Yutaka Taketani, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : 肝臓の脂質代謝を制御する胎生期栄養環境(会議録), Journal of the The Japan Diabetes Society, Vol.55, No.Supplement.1, S336, Apr. 2012.
72.	十河未来, Hironori Yamamoto, 香西美奈, 池田翔子, 中橋乙起, 大谷彩子, Yutaka Taketani and Eiji Takeda : 炎症性腸疾患の発症および治癒過程におけるリン摂取量の重要性(会議録), 第66回日本栄養・食糧学会大会講演要旨集, 151, Apr. 2012.
73.	中尾真理, Hironori Yamamoto, 中橋乙起, 池田翔子, 香西美奈, 田中更沙, Yutaka Taketani and Eiji Takeda : リン制限食摂取による腎性貧血の改善効果(会議録), 第66回日本栄養・食糧学会大会講演要旨集, 152, Apr. 2012.
74.	森本優香, 佐久間理英, 太田紘之, 梅田見名子, 石川真, Yutaka Taketani, Eiji Takeda and Hidekazu Arai : 24時間蓄尿を用いたリン摂取量の把握と妥当性の検討(会議録), 第66回日本栄養・食糧学会大会講演要旨集, 168, Apr. 2012.
75.	Hironori Yamamoto, 増田真志, 香西美奈, 池田翔子, 中橋乙起, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : レチノイン酸はIIb型リン酸トランスポーターNpt2b発現を抑制し小腸リン吸収を低下させる(会議録), 第66回日本栄養・食糧学会大会講演要旨集, 179, Apr. 2012.
76.	西正暁, Mitsuo Shimada, Hiroki Mori, Toru Utsunomiya, Satoru Imura, Yuji Morine, Tetsuya Ikemoto, Jun Hanaoka, 杉本光司, 齋藤裕, 山田眞一郎, 淺野間理仁, Hidenori Miyake, Eiji Takeda, Hisami Okumura, 佐々木一, 青沼広光 and 川島昭浩 : 肝切除周術期の生体侵襲に対するMEIN(R)投与の有用性の検討―基礎的実験と臨床的評価―, 第112回日本外科学会定期学術集会, Apr. 2012. (Keyword) 国内学会
77.	大谷彩子, Hironori Yamamoto, 香西美奈, 池田翔子, 中橋乙起, Yutaka Taketani, Tatsuya Tominaga, Toshio Doi and Eiji Takeda : リン·ビタミンD代謝異常による異所性石灰化発症の分子機構の解明, 第244回徳島医学会学術集会, Feb. 2012.
78.	中尾真理, Hironori Yamamoto, 中橋乙起, 池田翔子, 香西美奈, 田中更沙, Yutaka Taketani and Eiji Takeda : リン制限食による腎性貧血の改善効果, 第15回日本病態栄養学会年次学術集会, Jan. 2012.
79.	大南博和, Kikuko Amou, Yutaka Taketani, 佐藤佳瑞智, Hidekazu Arai, 小金井恵, 佐々木一, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : 食餌中の糖・脂質の異なる組合せがZucker fattyラットのインスリン感受性と骨格筋の脂肪酸組成に及ぼす影響, 第15回日本病態栄養学会年次学術集会, Jan. 2012.
80.	Rumi Katashima, 佐藤千穂, 丸笹美津子, 明石晃代, 高井繁美, 宮本登志子, 山上真樹子, Munehide Matsuhisa, Hiroshi Kitahata, Eiji Takeda, Hiro-omi Kanayama and Hiroaki Yanagawa : 徳島大学病院における臨床研究推進体制構築の試み, 第32回日本臨床薬理学会年会, Dec. 2011.
81.	向原理恵, Hironori Yamamoto, 中橋乙起, 池田翔子, 香西美奈, Yutaka Taketani and Eiji Takeda : 生体リン・ビタミンD代謝の概日リズムの分子機構, 第18回日本時間生物学会学術大会, Nov. 2011.
82.	Hironori Yamamoto and Eiji Takeda : エピジェネティクスと癌∼炎症と発癌，栄養食品因子について∼, 第33回日本臨床栄養学会総会第32回日本臨床栄養協会総会第9回大連合大会, Oct. 2011. (Keyword) Epigenetics / cancer
83.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : エピジェネティクスと糖尿病, 第33回日本臨床栄養学会総会第32回日本臨床栄養協会総会第9回大連合大会, Oct. 2011.
84.	大南博和, Wanjihia Violet, Yutaka Taketani, Kikuko Amou, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : 出生後の代謝応答を調節する胎児栄養状態の重要性, 第32回日本肥満学会, Sep. 2011.
85.	Yutaka Taketani, Takashi Uebanso, 大南博和 and Eiji Takeda : ヒトFGF21は絶食・飽食シグナルを感知する栄養代謝の変化に応答する因子である, 第32回日本肥満学会, Sep. 2011.
86.	堀江大輔, 山田歩規代, Ayako Tanimura, Yutaka Taketani, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : Na依存性リン酸トランスポーターとezrinとの新たな相互作用, 第84回日本生化学会, Sep. 2011.
87.	Yutaka Taketani, Hironori Yamamoto, Hisami Okumura, Ken-ichi Miyamoto and Eiji Takeda : 慢性腎臓病モデルラットにおけるリン接種制限による血管内皮機能改善効果, 第58回日本栄養改善学会学術総会, Sep. 2011.
88.	Yutaka Taketani, ヴヴァンタン, Ken-ichi Miyamoto, Hironori Yamamoto and Eiji Takeda : リン制限食はアデニン誘発性CKDモデルラットにおける血管内皮機能障害を改善する, 第29回日本骨代謝学会学術集会, Jul. 2011.
89.	Hironori Yamamoto, 増田真志, 香西美奈, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : レチノイン酸はIIb型リン酸トランスポーターNpt2b発現を抑制し小腸リン吸収を低下させる, 第29回日本骨代謝学会学術集会, Jul. 2011.
90.	Hironori Yamamoto, 池田翔子, 増田真志, 香西美奈, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : 敗血症時におけるリン代謝異常の分子メカニズムの解析, 第29回日本骨代謝学会学術集会, Jul. 2011.
91.	Hironori Yamamoto, 増田真志, 田中更紗, 香西美奈, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : 1-II-12 All-transレチノイン酸は小腸からのリン吸収を抑制する(一般演題要旨,日本ビタミン学会第63回大会講演要旨), Vitamins, Vol.85, No.4, 218, Jun. 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205784275840 (CiNii: 1390001205784275840)
92.	大谷彩子, Hironori Yamamoto, 竹井悠一郎, 香西美奈, Yutaka Taketani and Eiji Takeda : 2-II-28 Klotho変異マウスにおけるビタミンD合成酵素CYP27B1発現と異所性石灰化発生機序の解明(一般演題要旨,日本ビタミン学会第63回大会講演要旨), Vitamins, Vol.85, No.4, 254, Jun. 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205784435712 (CiNii: 1390001205784435712)
93.	Akira Nii, Mitsuo Shimada, Toru Utsunomiya, Satoru Imura, Yuji Morine, Tetsuya Ikemoto, Jun Hanaoka, 岩橋衆一, 斎藤裕, 山田眞一郎, 浅野間理仁, Hidenori Miyake, Eiji Takeda, Hisami Okumura, 佐々木一, 青沼広光 and 川島昭浩 : 肝切除周術期MEINR投与の有用性についての検討 : 基礎的実験とRCT(PS-206 ポスターセッション(206)肝臓:周術期管理-1,第111回日本外科学会定期学術集会), Journal of Japan Surgical Society, Vol.112, No.1, 863, May 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573668926805901568 (CiNii: 1573668926805901568)
94.	田中輝実, Van Vu Tan, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : アデニン誘導性CKDモデルラットにおける食事性リン制限は血管内皮機能を改善する, 第65回日本栄養・食糧学会大会, May 2011.
95.	中橋乙起, Hironori Yamamoto, 田中更沙, 向原理恵, 池田翔子, 橋本脩平, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : リン制限食によるFibroblast growth factor 15遺伝子発現調節機構, 第65回日本栄養・食糧学会大会, May 2011.
96.	Hironori Yamamoto, 増田真志, 香西美奈, 中橋乙起, 池田翔子, Yutaka Taketani, Hiroko Segawa, Ken-ichi Miyamoto and Eiji Takeda : レチノイン酸受容体RAR/RXRを介したナトリウム依存性リン酸輸送担体遺伝子の発現調節機構, 第65回日本栄養・食糧学会大会, May 2011.
97.	Eiji Takeda and Hisami Okumura : 臨床栄養管理からみた食事摂取法のエビデンス, 第14回日本病態栄養学会, Jan. 2011.
98.	Hironori Yamamoto, 菊地浩子, 中尾真理, 中橋乙起, 池田翔子, 田中更沙, Yutaka Taketani and Eiji Takeda : 腎不全における腸管鉄代謝異常の分子メカニズムの解明, 第14回日本病態栄養学会年次学術集会, Jan. 2011.
99.	川上由香, Hisami Okumura, 森由佳, 足立知咲, 佐久間理英 and Eiji Takeda : DNAチップを用いた食品負荷による食後高血糖の網羅的遺伝子発現評価, 第14回日本病態栄養学会, Jan. 2011.
100.	Hisami Okumura, 寺本有紗, 山内利香, 浦野恵利 and Eiji Takeda : 関節熱量計を用いずに肝疾患患者のLESの適応を判断するのに必要なnpRQを予測する血液生化学指標と式の検討, 第14回日本病態栄養学会, Jan. 2011.
101.	Hironori Yamamoto, 香西美奈, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : 甲状腺疾患におけるビタミンD代謝異常の分子メカニズムの解明, 第28回小児代謝性骨疾患研究会, Dec. 2010.
102.	Hiroki Mori, Mitsuo Shimada, 浅野間理仁, 山田眞一郎, 斎藤裕, 岩橋衆一, Jun Hanaoka, Tetsuya Ikemoto, Satoru Imura, Yuji Morine, Toru Utsunomiya, Hisami Okumura and Eiji Takeda : 肝切除周術期管理としての呼吸商の意義, 第72回日本臨床外科学会総会, Nov. 2010.
103.	中橋乙起, Hironori Yamamoto, 田中更紗, 増田真志, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : リン制限及び活性型ビタミンDによるFibroblast growth factor15遺伝子発現調節, 第43回日本栄養・食糧学会中国四国支部大会, Nov. 2010.
104.	Hironori Yamamoto, 佐々木一 and Eiji Takeda : パラチノースとオレイン酸の組合せ食による肥満モデルラットの糖·脂質代謝異常抑制効果, JDDW2010(第41回日本消化吸収学会総会・第18回日本消化器関連学会), Oct. 2010.
105.	Hisami Okumura, 山内利香, 浦野恵利 and Eiji Takeda : 間接熱量計を用いずに肝疾患患者のLES適応を評価する血液生化学指標の検討, 第32回日本臨床栄養学会総会第31回日本臨床栄養協会総会第8回大連合大会, Aug. 2010.
106.	Hironori Yamamoto, 香西美奈, Yutaka Taketani, Eiji Takeda, Ken-ichi Miyamoto and 加藤茂明 : 1.甲状腺疾患におけるリン・ビタミンD代謝異常の分子メカニズムの解明(第326回会議研究発表要旨,脂溶性ビタミン総合研究委員会), Vitamins, Vol.84, No.8, 408, Aug. 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205701667456 (CiNii: 1390001205701667456)
107.	Hironori Yamamoto, 香西美奈, 竹井悠一郎, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : 甲状腺ホルモン受容体β1を介したビタミンD-1α水酸化酵素(SYP27B1)遺伝子の転写抑制機構, 第28回日本骨代謝学会学術集会, Jul. 2010.
108.	Hironori Yamamoto, 竹井悠一郎, 佐藤匡俊, Yutaka Taketani and Eiji Takeda : Klotho-FGF23シグナル異常によるスタニオカルシン2の発現亢進と血管平滑筋細胞のリン酸誘導性石灰化の抑制, 第28回日本骨代謝学会学術集会，東京，平成22年7月21日~23日, Jul. 2010.
109.	Hironori Yamamoto, 香西美奈, 竹井悠一郎, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : 甲状腺ホルモン受容体β1を介したビタミンDー1α水酸化酵素(CYP27B1)遺伝子の転写抑制機構, 第28回日本骨代謝学会学術集会，東京，平成22年7月21日~23日, Jul. 2010.
110.	斎藤裕, Mitsuo Shimada, 浅野間理仁, 山田眞一郎, 岩橋衆一, Jun Hanaoka, Hiroki Mori, Tetsuya Ikemoto, Yuji Morine, Toru Utsunomiya, Hisami Okumura and Eiji Takeda : 肝傷害患者における術前栄養指標としての呼吸商の意義, 第47回日本外科代謝栄養学会学術集会, Jul. 2010.
111.	中橋乙起, Hironori Yamamoto, 池田翔子, 田中更沙, 竹井悠一郎, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : リン代謝異常および食餌性リンによる線維芽細胞増殖因子23(FGF23)の発現変動の解析, 第62回日本ビタミン学会大会,盛岡,平成22年6月11日~12日, Jun. 2010.
112.	増田真志, Hironori Yamamoto, 香西美奈, 石黒真理子, 中橋乙起, 田中更沙, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : 腎II型ナトリウム依存性リン酸輸送担体Npt2aを介した新規ビタミンD代謝調節機構, 第62回日本ビタミン学会大会，盛岡，平成22年6月11日~12日, Jun. 2010.
113.	Hironori Yamamoto, 浦川千鶴, 香西美奈, 増田真志, 中橋乙起, Yutaka Taketani, 山本雅之 and Eiji Takeda : 食餌性リンはNuclear factor-E2-related factor 2 (Nrf2)活性化を介し，腸管解毒遺伝子の発現を調節する, 日本分子生物学会第10回春季シンポジウム, Jun. 2010.
114.	大谷彩子, Hironori Yamamoto, 竹井悠一郎, 香西美奈, Yutaka Taketani and Eiji Takeda : Klotho変異マウスにおけるビタミンD合成酵素CYP27B1発現と異所性石灰化発生機序の解明, 日本分子生物学会第10回春季シンポジウム, Jun. 2010.
115.	Kikuko Amou, 大南博和, Yutaka Taketani, 佐藤佳瑞智, 深谷牧子, 上番増喬, Hidekazu Arai, 小金井恵, 佐々木一, Hironori Yamamoto and Eiji Takeda : 糖・脂肪毒性の相互作用を介した膵β細胞障害の発症機序の解明, 第53回日本糖尿病学会学術集会, May 2010.
116.	Kikuko Amou, 大南博和, Yutaka Taketani, 佐藤佳瑞智, 深谷牧子, 上番増喬, Hidekazu Arai, 小金井恵, 佐々木一, Hironori Yamamoto and Eiji Takeda : 膵β細胞障害の発症に対する食餌性糖・脂質の組み合せによる効果, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
117.	大南博和, Kikuko Amou, Yutaka Taketani, 上番増喬, 佐藤佳瑞智, 深谷牧子, Hidekazu Arai, 小金井恵, 佐々木一, Hironori Yamamoto and Eiji Takeda : 組織中の脂肪酸組成とインスリン抵抗性に及ぼす食餌中の糖・脂質の組合せの影響, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
118.	Ayako Tanimura, 鎌田歩規代, Yutaka Taketani, 斎藤亮彦, 堀江大輔, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : 血清リン濃度調節に関わるナトリウム依存性リン酸トランスポーターNaPi-IIa複合体の構造と機能, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
119.	Yutaka Taketani, Emi Shuto, Ken-ichi Miyamoto and Eiji Takeda : --, シンポジウム・第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
120.	Ayako Tanimura, 鎌田歩規代, Yutaka Taketani, 斎藤亮彦, 堀江大輔, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : 血清リン濃度調節に関わるナトリウム依存性リン酸トランスポーターNaPi-IIa複合体の構造と機能, 第64回日本栄養・食糧学会大会, May 2010.
121.	中橋乙起, Hironori Yamamoto, 田中更紗, Masashi Masuda, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : Fibroblast Growth Factor15遺伝子の発現に及ぼす食餌性リン及び活性型ビタミンD3の影響, 第64回日本栄養・食糧学会大会, May 2010.
122.	池田翔子, Hironori Yamamoto, 増田真志, 中橋乙起, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : 敗血症におけるリン代謝異常の分子メカニズムの解析．, 第64回日本栄養・食糧学会大会, May 2010.
123.	Asuka Shiota, Yutaka Taketani, 田中輝実, Masataka Sata, Hironori Yamamoto and Eiji Takeda : -, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
124.	池田翔子, Hironori Yamamoto, 増田真志, 中橋乙起, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : 敗血症におけるリン代謝異常の分子メカニズムの解析, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
125.	Emi Shuto, Yutaka Taketani, 大屋美穂, 小河真理子, 中西美咲, Kikuko Amou, Toshio Hosaka, Hironori Yamamoto, Tohru Sakai and Eiji Takeda : ヒトにおける食事性高リン負荷による血管内皮機能への影響, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
126.	Rie Mukai, 藤倉温, Takeshi Nikawa, Hironori Yamamoto, Eiji Takeda and Junji Terao : 廃用性筋萎縮モデルマウスにおけるケルセチンの筋重量低下抑制効果, 日本農芸化学会2010年度大会, Mar. 2010.
127.	浦野恵利, Hisami Okumura, 松本大, 山内利香, Mitsuo Shimada and Eiji Takeda : 肝疾患患者に対するテーラーメイド栄養管理の血液生化学指標についての検討, 第13回日本病態栄養学会年次学術集会, Jan. 2010.
128.	上番増喬, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, Hidekazu Arai, 竹井悠一郎, 増田真志, Ayako Tanimura, Nagakatsu Harada, Hisami Okumura and Eiji Takeda : FGF21はグルコースにより誘導される, 第13回日本病態栄養学会年次学術集会, Jan. 2010.
129.	Hironori Yamamoto, 菊地浩子, 桑原頌治, 田中更沙, 中橋乙起, Yutaka Taketani, Ken-ichi Miyamoto, 佐々木一 and Eiji Takeda : 腸管トランスポーターを分子標的とした腎疾患治療法の確立をめざして, 第13回日本病態栄養学会年次学術集会, Jan. 2010.
130.	Emi Shuto, Yutaka Taketani, Kikuko Amou, Toshio Hosaka, Hironori Yamamoto, Tohru Sakai and Eiji Takeda : 食事性のリン過剰摂取は血管内皮機能を障害する, 第13回日本病態栄養学会年次学術集会, Jan. 2010.
131.	Rie Mukai, 中尾玲子, Takeshi Nikawa, Hironori Yamamoto, Eiji Takeda and Junji Terao : マウス尾懸垂モデル系におけるケルセチンの筋萎縮抑制効果, 第14回日本フードファクター学会学術集会, Nov. 2009.
132.	Emi Shuto, Yutaka Taketani, Hironori Yamamoto, Tohru Sakai and Eiji Takeda : ヒトにおける食事性高リン負荷による血管内皮機能障害, 第63回日本栄養・食糧学会大会, May 2009.
133.	Emi Shuto, Yutaka Taketani, 田中理恵子, 一色政志, Kikuko Amou, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : ヒトにおける食事性高リン負荷による血管内皮機能障害, 第12回日本病態栄養学会年次学術集会, Jan. 2009.
134.	Emi Shuto, Yutaka Taketani, 一色政志, Hironori Yamamoto and Eiji Takeda : 高リン負荷による血管内皮機能障害, 第26回日本骨代謝学会学術集会, Oct. 2008.
135.	Emi Shuto, Yutaka Taketani, Hironori Yamamoto, Hisami Okumura, Tohru Sakai and Eiji Takeda : 食後高リン血症は血管内皮機能障害を惹起し心血管疾患のリスクとなる, 第55回栄養改善学会学術総会, Sep. 2008.
136.	Eiji Takeda : 臨床栄養学からみた炎症性腸疾患, 日清キョーリン製薬株式会社講演, Mar. 2006.
137.	Eiji Takeda : 子どもの歯の健康管理と栄養について, 徳島県鴨島保健所講演, Dec. 2005.
138.	Eiji Takeda : 栄養・食生活と生活習慣病, 学際企画株式会社講演, Dec. 2005.
139.	西田由香, Hisami Okumura, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : 急性高リン負荷によるFGF23の応答, 中外製薬株式会社講演, Dec. 2005.
140.	西田由香, Hisami Okumura, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : 急性の高リン負荷によるFGF23の応答, 小児代謝性骨疾患研究会, Vol.23, Dec. 2005.
141.	澤田直樹, Yutaka Taketani, 梨木邦剛, Hironori Yamamoto, Hidekazu Arai and Eiji Takeda : 基質小胞形成におけるカベリンの役割, 日本分子生物学会年会, Vol.28, Dec. 2005.
142.	Yutaka Taketani, 中村麻子, 梨木邦剛, 谷村綾子, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : Ezrinによるリン酸トランスポーター(NaPi-IIa)分子複合体の機能調節, 日本分子生物学会年会, Vol.28, Dec. 2005.
143.	Eiji Takeda : Regulatory mechanisms of inorganic phosphate homeostasis, 第53回国際歯科研究学会日本部会総会・学術大会, Nov. 2005.
144.	Eiji Takeda : 栄養成分と生体機能，SNPsと栄養, 第27回日本臨床栄養学会総会・第26回日本臨床栄養協会総会第Ⅲ回大連合大会, Nov. 2005.
145.	西田由香, Hisami Okumura, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : 高リン負荷に対するFGF23の応答, 徳島骨代謝研究会, Vol.12, Oct. 2005.
146.	E. Shuto, K. Nashiki, Yutaka Taketani, M. Isshiki, R. Tanaka, A. Tanimura, Y. Nishida, H. Okumura and Eiji Takeda : Inorganic phosphate mediates oxidative stress in bovine aortic endothelial cells, 日本生化学会大会, Vol.78, Oct. 2005.
147.	Yutaka Taketani, K. Nashiki, A. Nakamura, N. Sawada, Hironori Yamamoto, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Role of ezrin in the Downregulation of Sodium-Dependent Phosphate Transporter(NaPi-IIa) in Opossum Kidney Cells, 日本生化学会大会, Vol.78, Oct. 2005.
148.	Eiji Takeda : 食事・栄養によるストレス制御, 太陽化学株式会社講演, Sep. 2005.
149.	Eiji Takeda : 食事・栄養によるストレス制御, 国際「こころと栄養」シンポジウム, Sep. 2005.
150.	Eiji Takeda : 「腎疾患と栄養管理」「血液疾患と栄養管理」「感染・免疫・アレルギー疾患と栄養管理」, 日本栄養新報社講演, Sep. 2005.
151.	Hisami Okumura, 谷口章子, 西田由香, 竹内晴美, 首藤惠泉, Hidekazu Arai, Yutaka Taketani and Eiji Takeda : 粘性食品を組み合わせた朝食摂取による血糖値およびインスリン分泌への効果, 日本栄養改善学会学術総会, Vol.52, Sep. 2005.
152.	首藤惠泉, Yutaka Taketani, 西田由香, Hisami Okumura, Hidekazu Arai and Eiji Takeda : 高リン負荷による酸化ストレスと血管内皮機能障害, 日本栄養改善学会学術総会, Vol.52, Sep. 2005.
153.	Eiji Takeda : 「代謝性疾患と栄養管理」「内分泌・骨疾患と栄養管理」「呼吸器・循環器疾患と栄養管理」, 日本栄養新報社講演, Jul. 2005.
154.	Eiji Takeda : 栄養不良の病態と管理, さらや株式会社講演, Jul. 2005.
155.	辻光義, Hironori Yamamoto, 佐藤匡俊, Yutaka Taketani, 加藤茂明, 稲熊隆博 and Eiji Takeda : フラボノイド化合物ケルセチンの骨粗鬆症予防効果とその作用機構, 日本骨代謝学会学術集会, Vol.23, Jul. 2005.
156.	西田由香, Hisami Okumura, Yutaka Taketani, 佐藤匡俊, Hironori Yamamoto and Eiji Takeda : 単回リン負荷食の血中FGF-23濃度への影響, 日本骨代謝学会学術集会, Vol.23, Jul. 2005.
157.	Yutaka Taketani, 梨木邦剛, Hironori Yamamoto, 佐藤匡俊 and Eiji Takeda : IIa型ナトリウム依存性リン酸トランスポーター(NaPi-IIa)のエンドサイトーシスにおけるezrinの役割, 日本骨代謝学会学術集会, Vol.23, Jul. 2005.
158.	Eiji Takeda : 消化器疾患と栄養管理, 日本栄養新報社講演, Jun. 2005.
159.	Eiji Takeda : NSTについて, 徳島栄養士会講演, Jun. 2005.
160.	Eiji Takeda : 臨床栄養管理と食品機能評価, 太陽化学株式会社講演, Jun. 2005.
161.	Yutaka Taketani, K. Nashiki, N. Sawada, Hironori Yamamoto, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Role of ezrin in the parathyroid hormone-mediated downregulation of sodium-dependent phosphate transporter in opossum kidney cells, 日本細胞生物学会大会, Vol.58, Jun. 2005.
162.	Eiji Takeda : 「栄養アセスメント」「栄養補給法」「栄養摂取障害と栄養管理」, 日本栄養新報社講演, May 2005.
163.	Eiji Takeda : ナトリウム依存性リントランスポーターによるリン代謝調節機構, 旭化成ファーマ第40回日本小児腎臓病学会学術集会講演, May 2005.
164.	辻光義, Hironori Yamamoto, 佐藤匡俊, Yutaka Taketani, 庄子佳文子, 稲熊隆博 and Eiji Takeda : オニオン生理活性成分ケルセチンの骨粗鬆症予防効果, 日本ビタミン学会大会, Vol.57, May 2005.
165.	武藤佳瑞智, Hidekazu Arai, Akira Mizuno, 松尾薫, 深谷牧子, 小金井恵, 水本憲司, 麻生高伸, 有馬裕史, 佐々木一, Yutaka Taketani, Hironori Yamamoto, 土井俊夫 and Eiji Takeda : 内臓脂肪蓄積予防に対する糖・脂質形成の複合効果, 日本糖尿病学会年次学術集会, Vol.48, May 2005.
166.	竹井悠一郎, Hironori Yamamoto, 梨木邦剛, Yutaka Taketani and Eiji Takeda : スタニオカルシン2のビタミンD依存性分泌制御機構, 日本栄養・食糧学会大会, Vol.59, May 2005.
167.	石黒真理子, Hironori Yamamoto, 竹井悠一郎, Yutaka Taketani and Eiji Takeda : 甲状腺ホルモンによる生体リン代謝調節作用, 日本栄養・食糧学会大会, Vol.59, May 2005.
168.	山上文子, 津田紀子, 徳永圭代, Eiji Takeda, 川下圭一郎, 橋本忠幸, 木路修平 and 河野匡 : 陸上長距離選手のエネルギー代謝に関する研究, 日本栄養・食糧学会大会, Vol.59, May 2005.
169.	辻光義, Hironori Yamamoto, 佐藤匡俊, Yutaka Taketani, 庄子佳文子, 稲熊隆博 and Eiji Takeda : オニオン生理活性成分ケルセチンの骨粗鬆症予防効果, 日本栄養・食糧学会大会, Vol.59, May 2005.
170.	深谷牧子, Hidekazu Arai, Akira Mizuno, 松尾薫, Hisami Okumura, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 肝-門脈内グルコース感受性機構を介したインスリン分泌反応, 日本栄養・食糧学会大会, Vol.59, May 2005.
171.	谷口章子, Hisami Okumura, 西田由香, 竹内晴美, Hidekazu Arai, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 粘性食品を組み合わせた朝食摂取による血糖およびインスリン反応への効果, 日本栄養・食糧学会大会, Vol.59, May 2005.
172.	梨木邦剛, 首藤惠泉, 西田由香, Hisami Okumura, Hidekazu Arai, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 高リンによる酸化ストレスを介した血管内皮細胞機能障害, 日本栄養・食糧学会大会, Vol.59, May 2005.
173.	谷口章子, Hisami Okumura, 西田由香, 竹内晴美, Hidekazu Arai, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 粘性食品を組み合わせた朝食摂取による血糖およびインスリン反応, 日本栄養アセスメント研究会, Vol.28, May 2005.
174.	Eiji Takeda : 「病態栄養学の概念と意義」「生活習慣病と臨床栄養学」「栄養素の代謝と作用」「食事摂取基準・必要量」, 日本栄養新報社講演, Apr. 2005.
175.	Eiji Takeda : 「腎疾患と栄養管理」「血液疾患と栄養管理」「感染・免疫・アレルギー疾患と栄養管理」, 日本栄養新報社講演, Mar. 2005.
176.	Eiji Takeda : 「代謝性疾患と栄養管理」「内分泌・骨疾患と栄養管理」「呼吸器・循環器疾患と栄養管理」, 日本栄養新報社講演, Feb. 2005.
177.	Hidekazu Arai, 佐久間理英, 須浪聖香, 松尾薫, 深谷牧子, 武藤佳瑞智, Akira Mizuno, 佐々木一, 有馬裕史, 水本憲司, Hisami Okumura, Yutaka Taketani and Eiji Takeda : 糖質調整流動食(インスロー)の脂肪燃焼促進効果, 日本静脈経腸栄養学会, Vol.20, Feb. 2005.
178.	Eiji Takeda : 消化器疾患と栄養管理, 日本栄養新報社講演, Jan. 2005.
179.	Eiji Takeda : 糖尿病の予防・治療と生活習慣, 第8回日本病態栄養学会ランチョンセミナー講演, Jan. 2005.
180.	松尾薫, Hidekazu Arai, 武藤佳瑞智, 深谷牧子, 佐久間理英, Akira Mizuno, 水本憲司, 麻生高伸, 有馬裕史, 佐々木一, Yutaka Taketani, 土井俊夫 and Eiji Takeda : 糖質調整流動食(Inslow)の長期投与による内臓脂肪蓄積に対する予防効果, 日本病態栄養学会, Vol.8, Jan. 2005.
181.	Hironori Yamamoto, 木村宏子, 辻光義, 石黒真理子, 竹井悠一郎, 佐藤匡俊, Ken-ichi Miyamoto, 白神俊幸, 田中裕子, Hidekazu Arai, Yutaka Taketani and Eiji Takeda : 腸管ペプチド輸送担体(PepT1)を分子標的とした新たな栄養補給法の開発, 日本病態栄養学会, Vol.8, Jan. 2005.
182.	Hisami Okumura, 竹内晴美, 中村多希, 藤井正彦, 三宅秀則, 島田光生 and Eiji Takeda : SF-36を用いた肝硬変患者におけるLES療法長期継続効果の検討, 日本病態栄養学会, Vol.8, Jan. 2005.
183.	Eiji Takeda : 「栄養アセスメント」「栄養補給法」, 日本栄養新報社講演, Dec. 2004.
184.	Eiji Takeda : 栄養・食生活と生活習慣病, 学際企画(独)国立健康・栄養研究所講演, Dec. 2004.
185.	Eiji Takeda : 栄養・食生活と生活習慣病, 学際企画(独)国立健康・栄養研究所講演, Nov. 2004.
186.	Hiroki Moriguchi, Tomiaki Morikawa, Kazuya Matsumoto, Hideki Nakanishi, Eiji Takeda, Takafumi Katayama and Takaaki Nose : 知識データベース「褥瘡ケアネット」の開発(第2報), 医療情報学24回連合大会論文集, 504-505, Nov. 2004.
187.	Eiji Takeda : 炎症性腸疾患に対する栄養管理の進歩, 日本消化吸収学会総会, Vol.35, Oct. 2004.
188.	Eiji Takeda : 昼食後耐糖能におよぼす朝食での糖質調整流動食(インスロー)摂取の効果, 日本消化吸収学会総会, Vol.35, Oct. 2004.
189.	Hisami Okumura, 竹内晴美, 西田由香, 谷口章子, Hidekazu Arai, Yutaka Taketani and Eiji Takeda : SF-36を用いた肝硬変患者におけるLES療法長期継続効果の検討, 日本栄養改善学会学術総会, Vol.51, Oct. 2004.
190.	Eiji Takeda, 竹内里美, 竹内晴美, Hisami Okumura, Hidekazu Arai, Yutaka Taketani, 山田静恵 and 高橋保子 : 血清アルブミン濃度からみたNST活動の意義と改善点, 日本栄養・食糧学会中国・四国支部大会, Vol.37, Oct. 2004.
191.	佐久間理英, Hidekazu Arai, 須波聖香, 松尾薫, 深谷牧子, 武藤佳瑞智, Akira Mizuno, 佐々木一, 有馬裕史, 水本憲司, Hisami Okumura, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 糖質調整流動食インスロー摂取後の2nd meal effectの検討, 日本栄養・食糧学会中国・四国支部大会, Vol.37, Oct. 2004.
192.	Yutaka Taketani, T. Takeichi, K. Nashiki, Hironori Yamamoto, N. Sawada, M. Ichikawa, Hidekazu Arai and Eiji Takeda : Identification of target molecule of PTH-mediated signal transduction pathway that lead to the endocytosis of type IIa sodium dependent phosphate transporter, 日本生化学会大会, Vol.77, Oct. 2004.
193.	Eiji Takeda, Yutaka Taketani and Hironori Yamamoto : 「高リンと血管内皮細胞機能」「リン酸トランスポーターの発現調節機構」, 第8回瀬戸内カンファレンス, Aug. 2004.
194.	Hironori Yamamoto, 佐藤匡俊, 庄子佳文子, 梨木邦剛, Yutaka Taketani, 稲熊隆博 and Eiji Takeda : オニオン生理活性成分であるケルセチンによる骨粗鬆症予防効果, 日本骨代謝学会学術集会, Vol.22, Aug. 2004.
195.	佐藤匡俊, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 不動に伴う腸管カルシウム吸収低下機序の解明, 日本骨代謝学会学術集会, Vol.22, Aug. 2004.
196.	Hironori Yamamoto, 梨木邦剛, Yutaka Taketani, 佐藤匡俊 and Eiji Takeda : 核内受容体を介したナトリウム依存性リン酸輸送担体遺伝子の腎特異的転写制御機構, 日本骨代謝学会学術集会, Vol.22, Aug. 2004.
197.	Yutaka Taketani, 梨木邦剛, 武市朋子, Hironori Yamamoto and Eiji Takeda : IIa型ナトリウム依存性リン酸トランスポーター(NaPi-IIa)活性調節におけるカベオラ様ドメインの役割:シグナル伝達と細胞骨格制御, 日本骨代謝学会学術集会, Vol.22, Aug. 2004.
198.	Eiji Takeda : 臨床栄養管理法, 海部病院学術研修会(へき地中核病院研修事業後援会) 講演, Jul. 2004.
199.	Eiji Takeda : 小児の発育と発達，生理，栄養, 社団法人愛媛県栄養士会講演, Jun. 2004.
200.	Eiji Takeda, Yutaka Taketani and Hidekazu Arai : 食後高血糖を抑制する機能性食品の開発, 日本小児科学会徳島地方会, Vol.122, Jun. 2004.
201.	Eiji Takeda : 臨床栄養管理法, 神戸薬科大学同窓会研修会講演, May 2004.
202.	辻光義, Hironori Yamamoto, 三木田愛, 佐藤匡俊, 庄子佳文子, Hidekazu Arai, Yutaka Taketani, 稲熊隆博 and Eiji Takeda : タマネギ生理活性成分であるケルセチンによる骨代謝調節, 日本ビタミン学会大会, Vol.56, May 2004.
203.	佐藤匡俊, 山本かおり, Hironori Yamamoto, Hidekazu Arai, Yutaka Taketani and Eiji Takeda : 不動に伴う小腸カルシウム吸収及びPTH-ビタミンD調節系への影響, 日本ビタミン学会大会, Vol.56, May 2004.
204.	竹内晴美, 竹内里美, Hisami Okumura, 中村多希, Hidekazu Arai, Yutaka Taketani, 三宅秀則, 田代征記 and Eiji Takeda : SF-36を用いた肝硬変患者におけるLES療法長期継続効果の検討, 日本栄養アセスメント研究会, Vol.27, May 2004.
205.	Yutaka Taketani, T. Takeichi, K. Nashiki, N. Sawada, Hironori Yamamoto, Hidekazu Arai and Eiji Takeda : Studies on the translocational regulation of phosphate transporter by PTH with reference to PKA,PKC, and ezrin, 日本細胞生物学会大会, Vol.57, May 2004.
206.	梨木邦剛, 武市朋子, Yutaka Taketani and Eiji Takeda : PTHによるナトリウム依存性リン酸トランスポーター(NaPi-IIa)のエンドサイトーシス調節機構, 日本栄養・食糧学会大会, Vol.58, May 2004.
207.	Hironori Yamamoto, 三木田愛, 辻光義, 佐藤匡俊, 山本かおり, 庄子佳文子, Hidekazu Arai, Yutaka Taketani, 稲熊隆博 and Eiji Takeda : タマネギ成分，ケルセチンの骨代謝調節作用, 日本栄養・食糧学会大会, Vol.58, May 2004.
208.	Hidekazu Arai, Akira Mizuno, 松尾薫, 武藤佳瑞智, 深谷牧子, 水本憲司, 麻生高伸, 有馬裕史, 佐々木一, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 糖質調整流動食(MHN-01;Insolw)の内臓脂肪蓄積防止効果, 日本栄養・食糧学会大会, Vol.58, May 2004.
209.	Hidekazu Arai, Akira Mizuno, 松尾薫, 武藤佳瑞智, 深谷牧子, 水本憲司, 麻生高伸, 有馬裕史, 佐々木一, Yutaka Taketani, 土井俊夫 and Eiji Takeda : 糖質調整流動食(MHN-01;Insolw)の長期投与における内臓脂肪蓄積予防, 日本糖尿病学会年次学術集会, Vol.47, May 2004.
210.	Eiji Takeda : 食と健康, 大塚食品株式会社質販店会講演, Apr. 2004.
211.	Eiji Takeda : 栄養管理法について, 四国NMCクラブ講演, Mar. 2004.
212.	Eiji Takeda : 肝疾患でみられる耐糖能障害の病態と栄養管理, 第10回「岩手の消化器臨床栄養懇話会」講演, Mar. 2004.
213.	Eiji Takeda : 栄養・食生活と生活習慣病, 学際企画株式会社講演, Feb. 2004.
214.	Eiji Takeda : 栄養・食生活と生活習慣病, 学際企画株式会社講演, Feb. 2004.
215.	Hidekazu Arai, Akira Mizuno, Yutaka Taketani, 佐々木一, 有馬裕史, 松浦基, 水本憲司, 一色宏之, 土井俊夫 and Eiji Takeda : 糖質調整流動食(Insolw)摂取後の日内変動に及ぼす影響について, 日本静脈経腸栄養学会, Vol.19, Jan. 2004.
216.	深谷牧子, 佐久間理英, Hidekazu Arai, Akira Mizuno, 松尾薫, 武藤佳瑞智, 佐々木一, 有馬裕史, 松浦基, 水元憲司, Yutaka Taketani, 土井俊夫 and Eiji Takeda : 糖質調整流動食(Inslow)摂取後の血糖上昇抑制効果の持続, 日本病態栄養学会年次学術集会, Vol.7, Jan. 2004.
217.	Eiji Takeda : 薬と飲食物相互作用・各種食品の活用について, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(6) 特別講演, Dec. 2003.
218.	Eiji Takeda : 栄養士に役立つ栄養アセスメント, 香川県栄養士学会講演, Dec. 2003.
219.	Eiji Takeda : 糖の代謝について, 第4回高知県病院栄養士協議会研修会講演, Dec. 2003.
220.	Hironori Yamamoto, Shevde NK, Eiji Takeda, DeLuca HF and JW Pike : 2-Methylene -19-nor-(20S)-1,25-dihydroxyvitamin D3, 小児代謝性骨疾患研究会, Vol.21, Dec. 2003.
221.	Eiji Takeda : 「栄養管理の意義と考え方」-栄養アセスメント・栄養補給方を中心に-, 第307回徳島県中部臨床研究会講演, Dec. 2003.
222.	Hiroki Moriguchi, Tomiaki Morikawa, Kazuya Matsumoto, Hideki Nakanishi, Eiji Takeda and Takafumi Katayama : 知識データベース「褥瘡ケアネット」の開発, 医療情報学23回連合大会論文集, 692-693, Nov. 2003.
223.	Eiji Takeda : 栄養管理法について, 四国NMCクラブ講演, Nov. 2003.
224.	Eiji Takeda : 最大骨量を規定する環境因子とビタミンD受容体遺伝子多型(シンポジウム), 第30回小児栄養消化器肝臓学会「脂溶性ビタミンの臨床」, Nov. 2003.
225.	Hiroki Moriguchi, Tomiaki Morikawa, Kazuya Matsumoto, Hideki Nakanishi, Eiji Takeda and Takafumi Katayama : 知識データベース「褥瘡ケアネット」の開発, 第23回医療情報学連合大会, Nov. 2003.
226.	M. Ichikawa, Yutaka Taketani, K. Kobayashi, K. Nashiki, N. Sawada and Eiji Takeda : ESTABLISHMENT OF THE ELISA SYSTEM FOR CAVEOLIN-1, 日本生化学会大会, Vol.76, Oct. 2003.
227.	Yutaka Taketani, N. Amizuka, C. Ogawa, N. Sawada, K. Nomoto and Eiji Takeda : CAVEOLIN IN THE MATRIX VESICLES RELEASED FROM OSTEOBLAST, 日本生化学会大会, Vol.76, Oct. 2003.
228.	Eiji Takeda : 栄養管理法について, 四国NMCクラブ講演, Sep. 2003.
229.	Yutaka Taketani, Hidekazu Arai, Hisami Okumura and Eiji Takeda : 平成13年度国民栄養調査からみた日本人リン摂取状況とこれからの栄養指導, 日本栄養改善学会学術総会, Vol.50, Sep. 2003.
230.	Eiji Takeda, Hisami Okumura, Hidekazu Arai and Yutaka Taketani : 肝硬変における耐糖能障害の病態, 日本栄養改善学会学術総会, Vol.50, Sep. 2003.
231.	津田紀子, Hisami Okumura, Eiji Takeda, 竹下ゆかり, 橋本忠幸, 木路修平, 島口勝裕, 河野匡 and 山上文子 : 陸上長距離選手のエネルギー消費量評価, 徳島医学会学術集会, Vol.227, Jul. 2003.
232.	Eiji Takeda : エネルギー・核酸の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(6) 特別講演, Jul. 2003.
233.	Eiji Takeda, Hidekazu Arai, Akira Mizuno, 松尾薫, 深谷牧子, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani and 土井俊夫 : 食後高血糖を抑制する新規機能性流動食の開発, 日本外科代謝栄養学会, Vol.40, Jul. 2003.
234.	Eiji Takeda : ビタミン・無機質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(5) 特別講演, Jun. 2003.
235.	佐藤匡俊, Kyoko Morita, 加堂有紀, Yutaka Taketani, 新居佳孝 and Eiji Takeda : 不動に伴うカルシウム吸収低下機構の検討, 日本ビタミン学会大会, Vol.55, May 2003.
236.	Eiji Takeda : 内分泌疾患・代謝栄養疾患・ビタミン欠乏症, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(3) 特別講演, May 2003.
237.	Hidekazu Arai, Akira Mizuno, 松尾薫, 深谷牧子, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani, Toshio Doi and Eiji Takeda : 糖尿病患者および耐糖能異常者における糖質調整流動食(MHN-01)の食後高血糖抑制効果, 日本糖尿病学会年次学術集会, Vol.46, May 2003.
238.	佐藤匡俊, Kyoko Morita, 加堂有紀, Yutaka Taketani, 新居佳孝 and Eiji Takeda : 不動に伴うメカニカルストレスの低下が小腸カルシウム吸収へ及ぼす影響, 日本栄養・食糧学会大会, Vol.57, May 2003.
239.	津田紀子, 竹下ゆかり, Hisami Okumura, 橋本忠幸, 木路修平, 島口勝裕, 河野匡, 山上文子 and Eiji Takeda : 陸上長距離選手のエネルギー消費量からみたエネルギー代謝の効率化, 日本栄養・食糧学会大会, Vol.57, May 2003.
240.	Hidekazu Arai, 松尾薫, 深谷牧子, Akira Mizuno, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani, Toshio Doi and Eiji Takeda : 糖質調整流動食(MHN-01)の食後高血糖抑制効果および糖質代謝改善効果, 日本栄養・食糧学会大会, Vol.57, May 2003.
241.	Eiji Takeda, Hidekazu Arai, 庄司有里, 粟根尚美, Akira Mizuno, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani and Toshio Doi : 糖尿病患者および耐糖能異常者における糖質調整流動食(MHN-01)の食後血糖抑制効果, 日本栄養・食糧学会大会, Vol.57, May 2003.
242.	Yutaka Taketani, 網塚憲生, 小川千春, 澤田直樹, 野本香 and Eiji Takeda : 骨芽細胞からの基質小胞形成にカベオラが関与する, 日本細胞生物学会大会, Vol.56, May 2003.
243.	Hidekazu Arai, 庄司有里, 粟根尚美, 深谷牧子, 松尾薫, Yutaka Taketani, Eiji Takeda, Akira Mizuno, Toshio Doi, 佐々木一, 有馬裕史, 松浦基 and 一色宏之 : 耐糖能異常および肥満の改善効果が期待できる新規流動食(MHN-01)の開発, 日本栄養アセスメント研究会, Vol.26, May 2003.
244.	Eiji Takeda : タンパク質・アミノ酸の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(4) 特別講演, Apr. 2003.
245.	Eiji Takeda : 脂質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(3) 特別講演, Apr. 2003.
246.	Eiji Takeda : 栄養管理法について, 四国NMCクラブ講演会講演, Mar. 2003.
247.	Eiji Takeda : 生活習慣病に対する機能性食品の開発, (株)徳島健康科学総合センター講演, Mar. 2003.
248.	Eiji Takeda : 生活習慣病予防について・肥満が体に及ぼす影響について, 牟岐町生活習慣病予防健康講座講演, Mar. 2003.
249.	Eiji Takeda : 機能性食品の人での評価, (財)四国産業・技術振興センター健康産業産学交流会講演, Mar. 2003.
250.	Eiji Takeda : 小児期からの健康づくり∼小児生活習慣病予防対策委員会の取り組みについて∼, 徳島県日和佐保健所小児生活習慣病予防のための研修会・小児生活習慣病予防部会講演, Mar. 2003.
251.	Eiji Takeda : 糖質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(2) 特別講演, Mar. 2003.
252.	Eiji Takeda : 代謝調節と遺伝子, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(1) 特別講演, Feb. 2003.
253.	Hidekazu Arai, Akira Mizuno, 佐々木一, 有馬裕史, 松浦基, 一色宏之, 土井俊夫 and Eiji Takeda : 糖質調整流動食(MHN-01)の食後高血糖抑制効果:ヒト単回投与成績，, 日本静脈経腸栄養学会, Vol.18, Feb. 2003.
254.	Eiji Takeda : 病後の保育と給食について, 徳島市私保連・給食担当者研究会講演, Jan. 2003.
255.	Eiji Takeda and Hisami Okumura : 臨床栄養管理からみた食事摂取法のエビデンス, 第14回日本病態栄養学会, Jan. 2003.
256.	Eiji Takeda : NSTと病院栄養士のこれから, 全国病院栄養士協議会中国・四国地区AMM 講演, Jan. 2003.
257.	Eiji Takeda, Akira Mizuno, Hidekazu Arai, 庄司有里, 粟根尚美, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani and 土井俊夫 : 耐糖能異常を示す経管栄養患者に対する糖質調整流動食(MHN-01)長期投与の効果, 日本病態栄養学会年次学術集会, Vol.6, Jan. 2003.
258.	Hidekazu Arai, Akira Mizuno, 庄司有里, 粟根尚美, 佐々木一, 有馬裕史, 松浦基, Yutaka Taketani, 土井俊夫 and Eiji Takeda : 糖質調整流動食(MHN-01)飲用後の血糖上昇抑制効果, 日本病態栄養学会年次学術集会, Vol.6, Jan. 2003.
259.	Eiji Takeda : 免疫力を高める食事と生活, あけぼの会徳島支部講演, Dec. 2002.
260.	Eiji Takeda : 慢性肝疾患の病態と栄養管理法, 第9回熊本肝炎友の会講演会, Nov. 2002.
261.	Eiji Takeda : 栄養アセスメント, 社団法人大分県栄養士会生涯学習(3年コース・5年コース)研修会講演, Nov. 2002.
262.	Eiji Takeda : 生き生きすごす食と生活, 藍住町社会福祉協議会福祉健康づくりの町フェスティバル講演, Nov. 2002.
263.	Eiji Takeda : 高齢者の栄養状態の評価(スクリーニング・アセスメント), 社団法人日本栄養士会全国病院栄養士協議会講演, Nov. 2002.
264.	梨木邦剛, Yutaka Taketani, Kyoko Morita and Eiji Takeda : 無機リン酸トランスポーターのカベオラへの局在, (社)日本栄養・食糧学会中国・四国支部大会, Vol.35, Nov. 2002.
265.	工藤美千代, 鶴尾美穂, 秋田賢子, 寺沢ミエコ, Hisami Okumura, Eiji Takeda and Daisuke Inoue : 肝疾患合併糖尿病患者への超速効型インスリン注射と4分割食併用の試み, 日本糖尿病学会中国四国地方会総会, Vol.40, Nov. 2002.
266.	久保田恵, 吉田繁子, 元永恵子, 宗包仁, Hidekazu Arai and Eiji Takeda : 岡山県在住閉経後女性のライフスタイルと骨折リスクの検討, 日本栄養改善学会学術総会, Vol.49, Nov. 2002.
267.	Yutaka Taketani, Hisami Okumura, Kyoko Morita, Hidekazu Arai and Eiji Takeda : 食料需給表からみた日本人リン摂取量の推移, 日本栄養改善学会学術総会, Vol.49, Nov. 2002.
268.	Eiji Takeda, Hidekazu Arai, Yutaka Taketani, Kyoko Morita and Hisami Okumura : 肝硬変患者における長期就寝前夜食療法の効果, 日本栄養改善学会学術総会, Vol.49, Nov. 2002.
269.	中村多希, Hisami Okumura, 津田紀子, Hidekazu Arai, Yutaka Taketani, 三宅秀則, 田代征記, Akira Mizuno, 土井俊夫 and Eiji Takeda : 肝硬変で見られる耐糖能障害の病態に関する研究, 日本臨床栄養学会, Vol.24, Nov. 2002.
270.	Yutaka Taketani, 梨木邦剛, 澤田直樹, Kyoko Morita and Eiji Takeda : カベオラを介した無機リン酸トランスポーターのホルモンによる調節, 日本生化学会大会, Vol.75, Oct. 2002.
271.	Eiji Takeda : 身体面の諸検査結果説明, 日和佐保健所健康対策係平成14年度小児生活習慣病予防教室「すこやか教室」講演, Aug. 2002.
272.	Eiji Takeda : 乳幼児の発育発達と栄養について, 徳島県保育事業連合会第34回保育夏期大学講演, Aug. 2002.
273.	Eiji Takeda : エネルギー・核酸の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(6) 特別講演, Aug. 2002.
274.	Eiji Takeda : 肝臓疾患の最新の知見, 社団法人石川県栄養士会講演, Aug. 2002.
275.	Eiji Takeda : 肥満と生活習慣病, 日和佐保健所健康対策係平成14年度小児生活習慣病予防教室「すこやか教室」, Jul. 2002.
276.	Eiji Takeda : 低Glycemic-Index食品は糖尿病予防および治療効果を有するか?, 徳島医学会学術集会, Jul. 2002.
277.	Eiji Takeda : スポーツにとっての栄養, 徳島県スポーツ栄養士協会講演, Jul. 2002.
278.	Eiji Takeda : ビタミン・無機質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(5) 特別講演, Jul. 2002.
279.	Yutaka Taketani, 野本真由美, Hironori Yamamoto, 一色政志, 加藤茂明 and Eiji Takeda : 無機リン酸による25-水酸化ビタミンD-1α水酸化酵素の発現調節, 日本骨代謝学会, Vol.20, Jul. 2002.
280.	Hidekazu Arai, 粟根尚美, 辻本雄介, 由類江那奈, Akira Mizuno, 土井俊夫 and Eiji Takeda : OLETFラットにおけるインスリン早期分泌障害と糖尿病発症との関連性, 日本栄養・食糧学会大会, Vol.56, Jul. 2002.
281.	粟根尚美, Hidekazu Arai, 由類江那奈, 辻本雄介, Akira Mizuno, 土井俊夫 and Eiji Takeda : 肝硬変における早期インスリン分泌反応の亢進-肝硬変モデル動物を使っての検討-, 日本栄養・食糧学会大会, Vol.56, Jul. 2002.
282.	中村多希, Hisami Okumura, 津田紀子, 三宅秀則, 田代征記 and Eiji Takeda : 肝硬変患者における就寝前夜食(Late Evening Snack:LES)療法の効果, 日本栄養・食糧学会大会, Vol.56, Jul. 2002.
283.	梨木邦剛, Yutaka Taketani, Kyoko Morita and Eiji Takeda : Ⅱ型Na+依存性リン酸トランスポーターの細胞膜上の局在とPTHによるエンドサイトーシス, 日本栄養・食糧学会大会, Vol.56, Jul. 2002.
284.	佐藤匡俊, Kyoko Morita, 大久保公美, Yutaka Taketani, 新居佳孝 and Eiji Takeda : 不動に伴う小腸カルシウム吸収低下機構の解析, 日本栄養・食糧学会大会, Vol.56, Jul. 2002.
285.	Eiji Takeda : 「脂質の代謝」「脂質代謝からみた栄養管理」, 島根県栄養士会生涯学習研修会講演, Jun. 2002.
286.	Eiji Takeda : 肝硬変患者における病態栄養, 味の素ファルマ株式会社講演, Jun. 2002.
287.	Eiji Takeda : タンパク質・アミノ酸の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(4) 特別講演, Jun. 2002.
288.	Eiji Takeda : 高脂血症のなりたちと予防法, 徳島市保健センター成人保健係講演, Jun. 2002.
289.	Eiji Takeda : 脂質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(3) 特別講演, Jun. 2002.
290.	Eiji Takeda : 糖質の代謝と障害, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(2) 特別講演, May 2002.
291.	中村多希, Hisami Okumura, 津田紀子, Akira Mizuno, 三宅秀則, 田代征記, 鶴尾美穂 and Eiji Takeda : 肝硬変患者に対する就寝前夜食(LES)療法の長期継続効果:エネルギー代謝および耐糖能異常の改善がみられた1症例, 日本栄養アセスメント研究会, Vol.25, May 2002.
292.	Hidekazu Arai, Akira Mizuno, 粟根尚美, Yoshihiko Noma, 土井俊夫 and Eiji Takeda : OLETFラットにおけるインスリン早期分泌障害と糖尿病発症との関連性, 日本糖尿病学会年次学術集会, Vol.45, May 2002.
293.	Eiji Takeda : 代謝調節と遺伝子, 株式会社日本栄養新報社クリニカルダイエティシャン研究会栄養代謝生化学講座(1) 特別講演, Apr. 2002.
294.	野本真由美, Yutaka Taketani, Hironori Yamamoto, 一色政志, 加藤茂明 and Eiji Takeda : 無機リン酸による25-水酸化ビタミンD-1α水酸化酵素の発現調節, 日本ビタミン学会大会, Vol.54, Apr. 2002.
295.	Eiji Takeda : 慢性疾患の病態代謝と栄養管理について∼糖尿病・肝疾患を中心に∼, 宮崎県栄養士会ステップアップセミナー, Mar. 2002.
296.	Eiji Takeda : 栄養学への招待, 桐蔭総合大学事業講演, Mar. 2002.
297.	Eiji Takeda : 慢性肝疾患の病態と栄養管理, 第21回山口県臨床栄養研究会, Feb. 2002.
298.	Eiji Takeda : 病院栄養士の専門性と卒後研究, 熊本県栄養士会栄養学公開セミナー, Jan. 2002.
299.	Eiji Takeda : 夢を実現される食生活∼忍び寄る生活習慣病, 徳島県立城東高等学校ドリカムセミナー, Dec. 2001.
300.	Eiji Takeda : 肝疾患から見た耐糖能障害, 第6回和歌山県生活習慣病懇話会, Nov. 2001.
301.	Eiji Takeda : 糖尿病と代謝:とくに食事と肝臓の役割, 第17回備後糖尿病セミナー, Nov. 2001.
302.	Hisami Okumura, 中村多希, 津田紀子, Eiji Takeda and Akira Mizuno : 肝癌を合併した肝疾患患者の末梢および肝糖取り込み率を検討した1例, 日本臨床栄養学会, Vol.23, Nov. 2001.
303.	中村多希, Hisami Okumura, 津田紀子, Eiji Takeda and Akira Mizuno : euglycemic hyperinsulinemic clamp with oral glucose load法(clamp-OGL法)を用いた肝硬変患者における耐糖能異常の検討, 日本臨床栄養学会, Vol.23, Nov. 2001.
304.	久保田恵, 吉田繁子, 元永恵子, Hidekazu Arai, Eiji Takeda and 宗包仁 : 未閉経女性の骨密度に及ぼすVDR遺伝子多型とカルシウム摂取量との関連について, 日本臨床栄養学会, Vol.23, Nov. 2001.
305.	Eiji Takeda : 高齢者における病態別栄養管理, 阿南市医師会学術講演会講演, Oct. 2001.
306.	Hisami Okumura and Eiji Takeda : 肝癌を合併した肝疾患患者の末梢および肝糖取り込み率を検討した1例, 日本栄養改善学会, Vol.48, Oct. 2001.
307.	Eiji Takeda and Hidekazu Arai : ビタミンD受容体の腸管特異的発現調節部位の遺伝子多型と骨粗鬆症, 日本消化吸収学会総会, Vol.32, Oct. 2001.
308.	Eiji Takeda : 経腸栄養からみた栄養管理, 社団法人石川県栄養士会講演, Sep. 2001.
309.	Eiji Takeda : 高齢者における病態別栄養管理, 徳島市医師会講演, Sep. 2001.
310.	Eiji Takeda : これからの医療と管理栄養士の在り方及びその教育をめぐって, 静岡県立大学食品栄養科学講演, Sep. 2001.
311.	Eiji Takeda : 高齢者における病態別栄養管理, 板野郡医師会学術講演講演, Aug. 2001.
312.	Eiji Takeda : 「糖尿病予防に対する栄養士の役割」「糖尿病患者の栄養管理」, 大分県栄養士会生涯学習研修会, Aug. 2001.
313.	Eiji Takeda : カルシウム・ビタミンDと骨代謝, 野口病院生涯教育セミナー, Aug. 2001.
314.	Hironori Yamamoto, 小林くみ, Yutaka Taketani, Kyoko Morita, Hidekazu Arai, Eiji Takeda and 加藤茂明 : 腎近位尿細管IIa型ナトリウム依存性リン輸送担体の1α,25(OH)2D3による遺伝子発現制御機構の解析, 日本骨代謝学会, Vol.19, Aug. 2001.
315.	宮内章光, 高木康行, 吉本祥生, Ken-ichi Miyamoto, Eiji Takeda, 杉本利嗣, 山本威久, 千原和夫, M. J. Econs and H. Jueppner : 腫瘍性骨軟化症の惹起物質についての研究(FGF23の関与), 日本骨代謝学会, Vol.19, Aug. 2001.
316.	飯田めぐみ, Kyoko Morita, Hironori Yamamoto and Eiji Takeda : Cl-チャネルを介した新たなリン輸送制御経路, 日本骨代謝学会, Vol.19, Aug. 2001.
317.	Eiji Takeda : 高齢者における病態別栄養管理-栄養不良，糖尿病，慢性肝疾患について-, 東海神経内科栄養研究会, Vol.2, Jul. 2001.
318.	Eiji Takeda : 生活習慣病を予防する小児の健康保持と栄養管理, 学校保険委員会講演, Jun. 2001.
319.	Eiji Takeda : 糖質の代謝と調節，糖質と疾患, 社団法人島根県栄養士会生涯学習研修会講演, Jun. 2001.
320.	Eiji Takeda : 栄養管理のための栄養評価法, 社)徳島県栄養士会病院栄養士協議会研修会講演, May 2001.
321.	芳田美智子, Hironori Yamamoto, Kyoko Morita and Eiji Takeda : スタニオカルシン2の特性および分泌制御機構, 日本ビタミン学会大会, Vol.53, May 2001.
322.	Eiji Takeda : 「生活習慣病を問い直す-環境かゲノムか」骨代謝, 日本栄養食糧学会大会, Vol.55, May 2001.
323.	田口華代, Hisami Yamanaka, 中村多希, 高橋保子, 三宅秀則, 田代征記, 山上文子, 河野匡 and Eiji Takeda : 24時間心拍数法を用いた慢性肝疾患患者のエネルギー消費量, 日本栄養食糧学会大会, Vol.55, May 2001.
324.	小林くみ, Hironori Yamamoto, 谷佳子, Yutaka Taketani, Kyoko Morita, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : 腎近位尿細管におけるリン再吸収調節機構の解析, 日本栄養食糧学会大会, Vol.55, May 2001.
325.	Ken-ichi Miyamoto, 新居智子, Hiroko Segawa, Mikiko Ito, Yutaka Taketani, Eiji Takeda, 金井好克 and 遠藤仁 : CD98を介するアミノ酸輸送と感受システムの誘導機序, 日本栄養食糧学会大会, Vol.55, May 2001.
326.	Eiji Takeda : 健康増進に対する栄養士の貢献, 静岡英和女学院短期大学食物学科特別講演, Apr. 2001.
327.	Eiji Takeda : 慢性肝疾患の病態栄養管理, 城北臨床栄養カンファレンス特別講演, Vol.8, Apr. 2001.
328.	Eiji Takeda : 慢性肝疾患の病態と栄養管理, 栄養サポートチーム研究会講演, Mar. 2001.
329.	中村多希, Hisami Yamanaka, 田口華代, 粟根尚美, Akira Mizuno, 土井俊夫 and Eiji Takeda : インスリンクランプ法に経口血糖負荷試験を併用した方法(clamp-OGL)を用いた肝硬変患者における耐糖能異常の検討, 日本病態栄養学会, Vol.4, Jan. 2001.

Et cetera, Workshop:

1.	Masashi Masuda, Hironori Yamamoto, Yimamu Yilimulati, 大谷彩子, 大西里奈, Eiji Takeda and Yutaka Taketani : 第2回 Neo Vitamin D Workshop 学術集会, Aug. 2016.
2.	Hisami Okumura, Yutaka Taketani and Eiji Takeda : 脂質摂取量の多い食習慣が嗜好性に及ぼす影響についての検討, 36th European Congress for Nutrition and Metabolism, Dec. 2014.
3.	Mami Kanamoto, Yasuhiro Hamada, Yutaka Nakaya, Eiji Takeda, Hisami Okumura, Toru Utsunomiya, Satoru Imura, Yuji Morine, Tetsuya Ikemoto, Yusuke Arakawa, Hiroki Mori and Mitsuo Shimada : NST介入による周術期栄養管理の有用性に関する検討, Journal of Japan Surgical Society, Vol.115, No.2, 782, Mar. 2014. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573105977706375936 (CiNii: 1573105977706375936)
4.	Sonoko Yasui, Yoshiko Tani, Taiki Furumoto, Shizue Yamada, Akiko Uebanso, Shuhei Hasimoto, Chisaki Adachi, Akiko Matsumura, Eiji Takeda, Yutaka Nakaya, Shinsuke Katoh and Yasuhiro Hamada : くも膜下出血患者における栄養管理がリハビリテーションに及ぼす影響, 第16回徳島脳卒中研究会, Feb. 2014.
5.	Eiji Takeda, Hironori Yamamoto, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, Yutaka Taketani, Tatsuya Tominaga and Toshio Doi : 局所的CYP27B1発現亢進による異所性石灰化, 第334回脂溶性ビタミン総合研究委員会, Mar. 2012.
6.	Hironori Yamamoto, 大谷彩子, 横山望, 香西美奈, Yutaka Taketani and Eiji Takeda : リン・ビタミンD代謝異常による異所性石灰化発症の分子機構, 第2回骨バイオサイエンス研究会, Jul. 2011.
7.	増田真志, Hironori Yamamoto, 香西美奈, 竹井悠一郎, 中橋乙起, 池田翔子, 大谷彩子, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : All-transレチノイン酸による腸管リン吸収への影響とそのメカニズム, 日本農芸化学会中四国支部第29回講演会/日本ビタミン学会中国・四国地区第1回講演会合同講演会, Jan. 2011.
8.	中橋乙起, Hironori Yamamoto, 田中更沙, 増田真志, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : リン制限及び活性型ビタミンDによるFibroblast growth factor 15遺伝子発現調節, 第43回日本栄養・食糧学会中国・四国支部大会, Nov. 2010.
9.	橋本脩平, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 生体ミネラルバランスが時計遺伝子の発現調節に与える影響, 第43回日本栄養・食糧学会中国・四国支部大会, Nov. 2010.
10.	Hironori Yamamoto, 菊地浩子, 田中更沙, 中橋乙起, 中尾真理, Yutaka Taketani, 安西尚彦 and Eiji Takeda : 腎不全における腸管鉄代謝異常の分子メカニズムの解明, 第5回トランスポーター研究会年会, Jul. 2010.
11.	Eiji Takeda, 佐久間理英 and 阿望幾久子 : 糖質調整流動食インスローの機能および効果, 第12回マンスリーフードリサーチ, No.638, 12-16, Aug. 2008.
12.	Eiji Takeda : 栄養・食品クロムの耐糖能改善効果について, 日本医事新報, No.4383, 94, Apr. 2008.
13.	Eiji Takeda : 小中学生の栄養・食事のあり方, 阿南市学校保健会・学校保健収録, No.18, 18-25, 2008.
14.	Hisami Okumura, 廣瀬美和, Eiji Takeda, Masaaki Uno and Shinji Nagahiro : NST症例におけるワルファリン治療に及ぼす経腸栄養剤のビタミンK含有量の影響の検討, Nutrition Support Journal, Vol.10, No.1, 27-30, 2008.
15.	Eiji Takeda : 徳島大学のストレス研究の現況, Dec. 2005.
16.	Eiji Takeda, Hidekazu Arai, M. Sakuma, Yutaka Taketani, Akira Mizuno, T. Doi, M. Koganei and H. Sasaki : Effects of palatinose-based liquid diet (Inslow) intake on substrate oxidation and second meal effect in healthy men, ESPEN27th, Aug. 2005.
17.	Eiji Takeda : 消化管を標的とした機能性食品の開発, 第12回栄養とくしま講演会「腸管の分子栄養学」∼長寿・宇宙食の開発から未来の食品素材探索まで∼, Mar. 2005.
18.	Eiji Takeda : 経腸栄養剤の素材と生体機能調節, メディカルレビュー社栄養評価と治療座談会, Mar. 2005.
19.	Eiji Takeda : ヒトによる食品の糖尿病リスク低減機能評価, 食品の安全性および機能性に関する総合研究推進会議・評議会, Feb. 2005.
20.	Eiji Takeda : ストレス制御と機能性食品の開発, 徳島大学大学院ヘルスバイオサイエンス研究部設立記念シンポジウム-COE拠点形成のさらなる発展をめざして-, Nov. 2004.
21.	Eiji Takeda : Effects of a novel palatinose based liquid formula with low glycemic index (Inslow) on gene expression in rats Vahouny _ ILSI Japan, 難消化性糖質国際シンポジウム, Sep. 2004.
22.	梨木邦剛, 武市朋子, Yutaka Taketani and Eiji Takeda : 副甲状腺ホルモン(PTH)によるナトリウム依存症リン酸トランスポーター(NAPi-IIa)のエンドサイトーシス調整機構, 徳島医学会学術集会, Vol.229, Aug. 2004.
23.	佐藤匡俊, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : 不動応答性腸管カルシウム吸収低下機序の解明, 中国・四国骨代謝研究会, Vol.14, Jul. 2004.
24.	Hironori Yamamoto, 佐藤匡俊, 山本かおり and Eiji Takeda : 不動に伴うビタミンD依存性腸管カルシウム吸収低下機構の解明, 脂溶性ビタミン総合研究委員会, Vol.304, Jul. 2004.
25.	Yutaka Taketani, 梨木邦剛, 武市朋子 and Eiji Takeda : PTHによるナトリウム依存症リン酸トランスポーターNaPi-IIaのエンドサイトーシス調整機構, カルシトニン/副甲状腺ホルモン研究会, Vol.3, Dec. 2003.
26.	Eiji Takeda, Kyoko Morita and 佐藤匡俊 : 重力負荷によって産生される新規カルシウム吸収促進因子の同定, 宇宙環境利用に関する公募地上研究平成14年度終了テーマ研究成果報告会, Aug. 2003.
27.	Eiji Takeda and Hidekazu Arai : 「糖尿病用流動食の機能評価」共同研究の結果報告および検討, Sep. 2002.
28.	Eiji Takeda, 野本真由美, Hironori Yamamoto, Yutaka Taketani, 一色政志 and 加藤茂明 : 無機リン酸による25-水酸化ビタミンD-1α水酸化酵素の発現調節, 脂溶性ビタミン総合研究委員会, Vol.297, Sep. 2002.
29.	Eiji Takeda : The role of vitamin D receptor In human diseases:vitamin D dependent rickets type and osteoporosis, 中国人民解放軍総合病院高齢者研究所講演, Jul. 2002.
30.	Yutaka Taketani, Eiji Takeda and Kyoko Morita : メンブレントラフィッキングによるリン輸送担体の細胞内局在化とホルモンによる調節, 腎性骨症研究会平成13年度研究報告会, Jun. 2002.
31.	野本真由美, Yutaka Taketani, Hironori Yamamoto and Eiji Takeda : 無機リン酸による1α水酸化酵素の発現調節, 小児代謝性骨疾患研究会, Vol.19, Dec. 2001.
32.	Eiji Takeda : 腎におけるNa/Pi transporter:カルシトニンによる調節機構, カルシトニン/副甲状腺ホルモン研究会, Vol.1, Dec. 2001.
33.	野本真由美, Hironori Yamamoto, Yutaka Taketani, Kyoko Morita and Eiji Takeda : 無機リン酸による1α水酸化酵素の発現調節, 徳島Bone Forum, Dec. 2001.
34.	Eiji Takeda : 腸管ペプチド吸収系の意義と機能調節, SPGフォーラム, Vol.36, Dec. 2001.
35.	Eiji Takeda : 重力負荷によって生産される新規カルシウム吸収促進因子の同定, 選定宇宙環境利用に関する公募地上研究中間評価・報告会, Nov. 2001.
36.	Eiji Takeda, 芳田美智子, Hironori Yamamoto and Kyoko Morita : スタニオカルシン2の分子機構, 発達腎研究会, Vol.10, Sep. 2001.
37.	Eiji Takeda, Hisami Yamanaka, 中村多希, 粟根尚美, Akira Mizuno and 田代征記 : 肝硬変患者の耐糖脳障害に関するアセスメント, 日本栄養アセスメント研究会, Vol.24, Jun. 2001.
38.	Eiji Takeda : 肝硬変患者のインスリン抵抗性に関する研究, 四国臨床栄養研究会, Vol.25, Mar. 2001.

Report:

1.	Eiji Takeda and Hisami Okumura : 糖尿病予防・治療のための食品の組み合わせ効果に関するヒト試験，Ⅲ-3ヒト試験等による生活習慣病・メタボリックシンドロームの予防機能の検証，食品・農産物の表示の信頼性確保と機能性解析のための基盤技術の開発-機能性-(食品・農産物の新たな機能性解析技術の開発), 平成20年度運営委員会報告農林水産省農林水産技術会議事務局独立行政法人農業・食品産業技術総合研究機構食品総合研究所, Feb. 2009.
2.	Kunitaka Nashiki, Yutaka Taketani, Emi Shuto, Rieko Tanaka, Ayako Tanimura, Naoki Sawada, Tadatoshi Sato, Yuichiro Takei, Hidekazu Arai, Hironori Yamamoto, Nagakatsu Harada and Eiji Takeda : Evaluation of anti-stress nutrients in the endothelial cells with fluorescence indicator, The Journal of Medical Investigation : JMI, Vol.52, No.Supplement, 295-296, Tokushima, Nov. 2005. (Summary) Oxidative stress has emerged as an important pathogenic factor in the development of long-term complications, such as hypertension, atherosclerosis, nephropathy, and cancer. Taking many antioxidants from natural food may be effective to prevent us from those diseases. We have attempted to evaluate the effect of improvement by dietary antioxidants on the endothelial dysfunction induced by hyperglycemia. Fluorescence indicators for reactive oxygen species and nitric oxide were employed to the evaluation. The combination of those fluorescence indicators could be powerful tool to evaluate the effect of anti-stress nutrients on both oxidative stress and endothelial dysfunction. (Keyword) Animals / Antioxidants / Aorta, Thoracic / Cattle / Cell Culture Techniques / Cells, Cultured / Dose-Response Relationship, Drug / Endothelium, Vascular / Fluorescent Dyes / glucose / Hyperglycemia / Microscopy, Confocal / nitric oxide / oxidative stress / reactive oxygen species / Time Factors (Tokushima University Institutional Repository) ● Metadata: 111585 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.52.295 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16366519 ● Summary page in Scopus @ Elsevier: 2-s2.0-30144439691 (Tokushima University Institutional Repository: 111585, DOI: 10.2152/jmi.52.295, PubMed: 16366519, Elsevier: Scopus)
3.	Eiji Takeda, Hidekazu Arai, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : Control of oxidative stress and metabolic homeostasis by the suppression of postprandial hyperglycemia, The Journal of Medical Investigation : JMI, Vol.52 Suppl, 259-265, Nov. 2005. (Summary) Repeated mental stress may lead to chronic alterations in cortisol and catecholamine concentrations and to insulin resistance. Furthermore, chronically elevated cortisol concentrations may favour the development of abdominal obesity and of the metabolic syndrome. Oxidative stress impairs glucose uptake in muscle and fat and correlates with BMI. Obese subjects with type 2 diabetes, especially soon after the onset of diabetes, usually exhibit postprandial hyperglycemia with delayed hyperinsulinemia. It is recognized that insulin resistance causes postprandial hyperglycemia; however, it is also possible that impairment of early insulin secretion in response to an oral glucose load is the reason why postprandial hyperglycemia occurs. Since even modest increases in postprandial glucose values can be a risk factor for cardiovascular disease. Therefore, the effects of palatinose based functional food which reduces postprandial hyperglycemia and hyperinsulinemia were investigated in rats. This novel food definitely reduced visceral fat accumulation and improved insulin sensitivity. Therefore, it is suggested that functional food which suppresses postprandial glucose level is beneficial for both stress and metabolic controls. (Keyword) Adipose Tissue / Animals / Area Under Curve / Blood Glucose / Body Mass Index / Body Weight / Cardiovascular Diseases / Dextrins / Enteral Nutrition / Epididymis / Food, Formulated / Glucose / Glucose Tolerance Test / Homeostasis / Humans / Hyperglycemia / Hyperinsulinism / Insulin / Insulin Resistance / Isomaltose / Male / Organ Size / Oxidative Stress / Postprandial Period / Rats / Rats, Sprague-Dawley / Risk Factors / Time Factors (Tokushima University Institutional Repository) ● Metadata: 111562 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.52.259 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16366512 ● Search Scopus @ Elsevier (PMID): 16366512 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.52.259 (Tokushima University Institutional Repository: 111562, DOI: 10.2152/jmi.52.259, PubMed: 16366512)
4.	Eiji Takeda : Human nutritional science on stress control, The Journal of Medical Investigation : JMI, Vol.52 Supplement, 223-224, Nov. 2005. (Summary) Severe and prolonged stress exposure impairs homeostatic mechanisms, particularly associated with the onset of depressive illness. The establishment of functional foods that correctly regulate stress response must be an important and new field for human nutrition. This exciting science has been vigorously achieving in the 21st century COE program of University of Tokushima Graduate School. (Keyword) health promotion / Humans / Models, Biological / Nutritional Physiological Phenomena / Socioeconomic Factors / Stress, Physiological / Suicide (Tokushima University Institutional Repository) ● Metadata: 111550 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.52.223 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16366501 ● Summary page in Scopus @ Elsevier: 2-s2.0-30144441702 (Tokushima University Institutional Repository: 111550, DOI: 10.2152/jmi.52.223, PubMed: 16366501, Elsevier: Scopus)
5.	Eiji Takeda : 臨床栄養管理に対する基礎的および実践的研究, 日本栄養・食糧学会誌, Vol.58, No.1, 23-28, 2005.
6.	Eiji Takeda and 佐々木一 : 昼食後耐糖能におよぼす朝食での糖質調整流動食(インスロー)摂取の効果, The Japanese Society of Digestion and Absorption, Vol.27, No.2, 20-21, 2004.
7.	Eiji Takeda : 栄養学について, 日本臨床栄養学雑誌, Vol.23, 3-4, 2001.

Patent:

1.	Yutaka Taketani and Eiji Takeda : 消化管粘膜保護剤，カベオリン遺伝子発現促進剤および抗ストレス剤, 2005319349 (Nov. 2005), 2007126383 (May 2007), 4839436 (Oct. 2011).

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Epigenomic modification by stress related nutrients (Project/Area Number: 24650423 )
Psychological, physiological and nutrition metabolic change from health to disease (Project/Area Number: 24300256 )
Development of multidisciplinary therapy based on mechanism of liver insufficiency in a use of Aged partial graft after liver transplantation. (Project/Area Number: 23390324 )
Association of food intake and epigenetics in life-style related diseases (Project/Area Number: 22650180 )
Nutritional functions and its organ metabolism network (Project/Area Number: 21300277 )
脂肪肝グラフト部分肝移植における機能不全の解明と統合的治療法の開発 (Project/Area Number: 20390359 )
Molecular bases of hypoglycemc index diet which prevents metabolic syndrome (Project/Area Number: 18300232 )
リン過剩摂取による食後高リン血症の概念の確立と病態の解明 (Project/Area Number: 17650225 )
Studies on the practical use of soybean peptides for oral health promotion in the elderly (Project/Area Number: 17592182 )
末梢血からの破骨細胞形成能を指標とした食品の抗ストレス機能評価 (Project/Area Number: 16659173 )
Complex phosphate sensing system regulating phosphate homeostasis (Project/Area Number: 13470013 )
The regulatory mechanism of phosphate transport activity mediated by sodium-dependent phosphate transporter (Project/Area Number: 11671038 )
Development of detection method for novel calcium- and phosphate- regulating hormone (phosphatonin) (Project/Area Number: 10557096 )
一回の膜貫通領域をもつアミノ酸輸送担体の分子構造および機能解析 (Project/Area Number: 09257233 )
遺伝子発現量を指標とした適正リン摂取量決定法に関する研究 (Project/Area Number: 08877071 )
一回の膜貫通域をもつアミノ酸輸送担体の分子構造と機能解析 (Project/Area Number: 08268236 )
Development of assay method of serum 1,25-dihydroxyvitamin D concentration without radioisotope (Project/Area Number: 07557321 )
一回の膜貫通領域をもつアミノ酸輸送担体の分子構造および機能解析 (Project/Area Number: 07276227 )
ビタミンD受容体のゲノム遺伝子解析とビタミンD受容体障害の簡易検出法の確立 (Project/Area Number: 06670800 )
Hypophosphatemia : cDNA cloning of a Na^+-dependent phosphate co-transporter from human kidney (Project/Area Number: 05670145 )
Molecular analysis of vitamin D receptor defect and regulation of expression of vitamin D action (Project/Area Number: 04670601 )
Molecular and gentic analysis of receptor for 1, 25-dihydroxyvitamin D in patients with vitamin D-dependent rickets type II (Project/Area Number: 02670444 )
Screening for disorders of pyruvate metabolism by measurement of lactate production in cultured skin fibroblasts (Project/Area Number: 63570441 )
Studies on pathogenesis and treatment of vitamin D-dependent rickets type II. (Project/Area Number: 62570428 )
Establishment of a rapid diagnosis of congenital lactic acidosis using peripheral blood samples (Project/Area Number: 61570459 )
先天性高乳酸血症の病因としてのピルビン酸膜輸送障害に関する研究 (Project/Area Number: 61219016 )
Research on DNA biosynthesis in human hematologic malignant cells. (Project/Area Number: 59570399 )
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Professor Emeritus : Takeda, Eiji

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)