徳島大学 / 教育研究者総覧 --- 竹谷豊

個人のホームページ

https://researchmap.jp/read0184062 (researchmap)

専門分野

○	骨ミネラル代謝学 (Bone and Mineral Metabolism)
○

研究テーマ

○	カルシウム·リン代謝の栄養学 (カルシウム (calcium), リン (phosphorus), 骨ミネラル代謝 (bone and mineral metabolism), 高リン血症 (hyperphosphatemia), 低リン血症 (hypophosphatemia)) (生体におけるカルシウムおよびリン代謝の調節機構の解明と栄養学的意義に関する研究を行っている．また，カルシウムおよびリン代謝異常による病態の解明と栄養管理法についても研究を行っている．)
○	糖脂質による腸管粘膜保護作用 (糖脂質, 腸管粘膜, カベオリン)

著書・論文

著書:

1.	加藤明彦 (内科学), 竹谷豊, 𦚰野修, 北島幸枝 : 腎臓栄養学, 朝倉書店, 2024年5月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1130581611739888006 (CiNii: 1130581611739888006)
2.	竹谷豊, 増田真志, 大南博和 : フィトケミカルの機能と作用メカニズム, 2023年6月.
3.	大南博和, 滝川真輝, 北村彩乃, 松原未奈, 竹谷豊 : エネルギー代謝の評価, 日本メディカルセンター, 2023年4月. (出版サイトへのリンク) ● Publication site (DOI): 10.19020/cd.0000002513 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390014337396806144 ● Search Scopus @ Elsevier (DOI): 10.19020/cd.0000002513 (DOI: 10.19020/cd.0000002513, CiNii: 1390014337396806144)
4.	竹谷豊, 塚原丘美, 桑波田雅士, 阪上浩 : 新・臨床栄養学第2版, 株式会社講談社, 東京, 2023年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1130014316335459844 (CiNii: 1130014316335459844)
5.	竹谷豊 : 個体の調節機能, 医歯薬出版株式会社, 東京, 2022年9月.
6.	武田英二, 竹谷豊, 新井英一, 阪上浩, 藤岡由夫, 細川雅也 : 臨床病態栄養学第4版, 文光堂, 東京, 2021年12月.
7.	増田真志, 山本浩範, 竹井悠一郎, 中橋乙起, 足立雄一郎, 大西康太, 大南博和, 奥村仙示, 阪上浩, 宮崎淳, 武田英二, 竹谷豊 : All-transレチノイン酸は腸管ナトリウム依存性リン酸トランスポーター遺伝子(Npt2b)の転写を負に制御する, 日本ビタミン学会, 2020年11月. (要約) 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． (キーワード) 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) (出版サイトへのリンク) ● Publication site (DOI): 10.20632/vso.94.11_545 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390571704642711680 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.94.11_545 (DOI: 10.20632/vso.94.11_545, CiNii: 1390571704642711680)
8.	坂井麻衣子, 大西康太, 増田真志, 大南博和, 奥村仙示, 原太一, 竹谷豊 : イソラムネチンはJ774.1マウスマクロファージ様細胞株においてTFEB非依存的にリソソームのタンパク質分解を促進, 2020年10月.
9.	多々納(福田) 詩織, 山本浩範, 中橋乙起, 吉川亮平, 林眞由, 岸本麻希, 伊美友紀子, 奥村仙示, 大西康太, 増田真志, 竹谷豊 : 成長期における食餌性リンによるα-klotho発現制御, 2020年6月.
10.	杉山茂, 森賀俊広, 加藤雅裕, 村井啓一郎, 堀河俊英, 霜田直宏, 古部昭広, 柳谷伸一郎, 小笠原正道, 山本孝, 中村嘉利, 浅田元子, 佐々木千鶴, 田中秀治, 竹内政樹, 竹谷豊, 奥村仙示, 増田真志, 岡本敏弘 : 枯渇資源と技術開発, --- 徳島大学における分野融合型枯渇資源対応技術の開発 ---, 徳島大学産業院出版部, 徳島, 2020年3月. (要約) 2017年度から徳島大学重点クラスター``人類の恒久的繁栄に向けた対枯渇資源対応技術の開発''として活動した成果を，一般の読者にもわかりやすいように公表した徳島大学産業院出版部から始めて出版した書籍である．
11.	増田真志, 新井田裕樹, 竹谷豊, 二川健 : ビタミンD欠乏とサルコペニアについて, 株式会社講談社, 東京, 2018年4月.
12.	竹谷豊, 伊美友紀子, 新井田裕樹 : リンとカルシウム, 2017年12月.
13.	竹谷豊, 楢﨑遙子, 伊美友紀子, 新居紗知 : 食事性リンと血管内皮機能障害, 医学図書出版株式会社, 2017年11月.
14.	竹谷豊 : サプリメント, 朝倉書店, 2017年11月.
15.	竹谷豊 : リンと尿路結石, 朝倉書店, 2017年11月.
16.	竹谷豊 : リンと筋疾患, 2017年11月.
17.	竹谷豊 : リフィーディング症候群, 朝倉書店, 2017年11月.
18.	竹谷豊 : 人体とリン, 朝倉書店, 2017年11月.
19.	竹谷豊 : 栄養障害, 株式会社中山書店, 2017年9月.
20.	竹谷豊 : ビタミン欠乏症・過剰症・依存症, 朝倉書店, 2017年3月.
21.	竹谷豊 : 食材によってリン吸収率に違いはありますか?, 株式会社中外医学社, 2016年6月.
22.	竹谷豊 : 呼吸器疾患, 株式会社講談社, 2016年1月.
23.	竹谷豊 : 臨床栄養学の概念, 株式会社講談社, 2016年1月.
24.	竹谷豊, 竹井悠一郎, 谷村綾子 : 微量元素・ビタミン不足の評価 (特集栄養障害患者の評価), 科学評論社, 2016年.
25.	生城浩子, 太田好次, 瀧谷公隆, 竹谷豊, 津川尚子, 堀尾文彦, 山田和子, 渡邊敏明 : 第3版ビタミン・ミネラルの安全性, 2014年9月.
26.	竹谷豊, 中尾真理 : CKD-MBDの管理における食事性リン, 2014年6月.
27.	竹谷豊, 増田真志 : リン摂取と循環器疾患, 2014年5月.
28.	竹谷豊, 大南博和 : リン不足および過剰と栄養, 2014年5月.
29.	武田英二, 奥村仙示, 中尾真理, 竹谷豊 : 抗ストレス効果を示す食品・食生活とバイオマーカー, 株式会社シーエムシー出版, 2013年9月.
30.	新井英一, 阪上浩, 武田英二, 竹谷豊, 藤岡由夫, 細川雅也 : 臨床病態栄養学第3版, 文光堂, 2013年9月.
31.	竹谷豊 : 栄養モニタリングと評価, 第一出版, 2012年9月.
32.	竹谷豊, 福澤健治 : ビタミン欠乏症, 西村書店, 2012年7月.
33.	Eiji Takeda, Hironori Yamamoto, Hisami Okumura and Yutaka Taketani : Complications and Managements of Hyperphosphatemia in Dialysis, InTech, Nov. 2011.
34.	竹谷豊 : ミネラル・微量元素のトランスポーター, 株式会社建帛社, 2011年5月.
35.	桑原頌治, 西山俊, 大井彰子, 金子一郎, 辰巳佐和子, 伊藤美紀子, 竹谷豊, 宮本賢一 : リン酸トランスポーター関連分子群とリン代謝異常症, メディカルドゥ社, 2011年3月.
36.	宮本賢一, 竹谷豊, 辰巳佐和子, 伊藤美紀子, 瀬川博子 : 無機リン酸イオンとトランスポーター, 京都廣川書店, 2011年3月.
37.	竹谷豊 : 食事摂取基準の活用, 株式会社朝倉書店, 2010年11月.
38.	竹谷豊 : 栄養管理におけるビタミンK, 株式会社朝倉書店, 2010年11月.
39.	武田英二, 竹谷豊 : 第1章2-C ストレスと栄養，最新栄養予防・治療学, 株式会社永井書店, 東京, 2007年1月.
40.	竹谷豊 : 第1章2-B 単身者，最新栄養予防・治療学, 株式会社永井書店, 東京, 2007年1月.
41.	武田英二, 岡久稔也, 高橋保子, 国清紀子, 松村晃子, 中屋豊, 西正晴, 竹谷豊, 吉本勝彦, 寺尾純二, 美馬福恵, 吉岡昌美, 山田静恵, 石澤啓介, 鈴木麗子, 藤田知代, 新井英一, 桑波田雅士, 岡田和子 : 栄養管理のチーム医療, 文光堂, 東京, 2006年4月.
42.	中屋豊, 桑波田雅士, 丹黒章, 土井俊夫, 竹谷豊, 野間喜彦, 武田英二, 東博之, 島田光生, 栗田信浩, 大森哲郎, 西正晴, 青野純典, 西岡安彦, 吉本勝彦, ほか 65名 : NST用語ハンドブック, メディカルレビュー社, 東京, 2006年2月.
43.	中屋豊, 宮本賢一, 坂巻路可, 乾明夫, 合田敏尚, 南久則, 川崎英二, 長田恭一, 佐藤隆一郎, 長澤孝志, 渡邊文雄, 岡達三, 桑波田雅士, 髙橋章, 竹谷豊 : エッセンシャル基礎栄養学, 医歯薬出版株式会社, 東京, 2005年11月.
44.	中屋豊, 鈴木和枝, 馬渡一諭, 桑波田雅士, 竹谷豊, 原田永勝, 山本浩範 : 臨床栄養学(第4版), 医学出版社, 東京, 2004年3月.
45.	庄司有里, 新井英一, 水野昭, 佐々木一, 水本憲司, 有馬裕史, 松浦基, 粟根尚美, 竹谷豊, 土井俊夫, 武田英二 : 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, 日本病態栄養学会, 2003年.

学術論文(審査論文):

1.	Yuki Mori, Masashi Masuda, Risa Yoshida-Shimizu, Saki Aoyagi, Yuichiro Adachi, The Anh Nguyen, Yusuke Maruyama, Yosuke Okumura, Yuki Kamei, Maiko Sakai, Kohta Ohnishi, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipophagy through the activation of the AMPK-Beclin1 signaling pathway and reduces Rubicon expression in adipocytes., The Journal of Nutritional Biochemistry, Vol.126, 2024. (要約) Lipophagy is defined as a lipolysis pathway that degrades lipid droplet (LD) via autophagy. All-trans retinoic acid (atRA), a metabolite of vitamin A, stimulates lipolysis through hormone-sensitive lipase and β-oxidation. However, the regulation of lipolysis by atRA-induced autophagy in adipocytes remains unclear. In this study, we investigated the effect of atRA on autophagy in epididymal fat of mice and the molecular mechanisms of autophagy in 3T3-L1 adipocytes. Western blotting showed that atRA decreased the expression of p62, a cargo receptor for autophagic degradation, and increased the expression of the lipidated LC3B (LC3B-II), an autophagy marker, in epididymal fat. Next, we confirmed that atRA increased autophagic flux in differentiated 3T3-L1 cells using the GFP-LC3-RFP-LC3ΔG probe. Immunofluorescent staining revealed that the colocalization of LC3B with perilipin increased in differentiated 3T3-L1 cells treated with atRA. The knockdown of Atg5, an essential gene in autophagy induction, partly suppressed the atRA-induced release of non-esterified fatty acid (NEFA) from LDs in differentiated 3T3-L1 cells. atRA time-dependently elicited the phosphorylation of AMPK and Beclin1, autophagy-inducing factors, in mature 3T3-L1 adipocytes. Inversely, atRA decreased the protein expression of Rubicon, an autophagy repressor, in differentiated 3T3-L1 cells and epididymal fat. Interestingly, the expression of ALDH1A1, atRA-synthesizing enzymes, increased in epididymal fat with decreased protein expression of Rubicon in aged mice. These results suggest that atRA may partially induce lipolysis through lipophagy by activating the AMPK-Beclin1 signaling pathway in the adipocytes and increased atRA levels may contribute to decreased Rubicon expression in the epididymal fat of aged mice. (248/250 words). (キーワード) Mice / Animals / AMP-Activated Protein Kinases / Beclin-1 / Signal Transduction / Lipolysis / Tretinoin / Autophagy / Adipocytes / 3T3-L1 Cells (徳島大学機関リポジトリ) ● Metadata: 119349 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2024.109589 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38295886 ● Search Scopus @ Elsevier (PMID): 38295886 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2024.109589 (徳島大学機関リポジトリ: 119349, DOI: 10.1016/j.jnutbio.2024.109589, PubMed: 38295886)
2.	Yosuke Okumura, Kotaro Abe, Shoko Sakai, Yuki Kamei, Yuki Mori, Yuichiro Adachi, Masaki Takikawa, Ayano Kitamura, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Taiho Kambe, Hironori Yamamoto and Yutaka Taketani : Elevated luminal inorganic phosphate suppresses intestinal Zn absorption in 5/6 nephrectomized rats., American Journal of Physiology, Renal Physiology, Vol.326, No.3, F411-F419, 2024. (要約) binder might be useful for the treatment of hypozincemia and hyperphosphatemia. (キーワード) Humans / Rats / Animals / Phosphates / Hyperphosphatemia / Zinc / Renal Insufficiency, Chronic / Nephrectomy / Intestinal Absorption (徳島大学機関リポジトリ) ● Metadata: 119347 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00310.2023 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38234299 ● Search Scopus @ Elsevier (PMID): 38234299 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00310.2023 (徳島大学機関リポジトリ: 119347, DOI: 10.1152/ajprenal.00310.2023, PubMed: 38234299)
3.	Shinta Nishioka, Yoji Kokura, Ryo Momosaki and Yutaka Taketani : Measures for Identifying Malnutrition in Geriatric Rehabilitation: A Scoping Review., Nutrients, Vol.16, No.2, 223, 2024. (要約) = 1). These findings highlight the need to distinguish the functional impairment of nutritional origin from that of non-nutritional origin in nutritional assessment procedures, and the need to study the accuracy and the predictive validity of these measures in geriatric rehabilitation patients. (キーワード) Humans / Aged / Nutrition Assessment / Nutritional Status / Malnutrition / Body Weight / Weight Loss (出版サイトへのリンク) ● Publication site (DOI): 10.3390/nu16020223 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38257116 ● Summary page in Scopus @ Elsevier: 2-s2.0-85183266621 (DOI: 10.3390/nu16020223, PubMed: 38257116, Elsevier: Scopus)
4.	Ayari Tsumura, Hisami Yamanaka-Okumura, Hana Kawakami, Shiori Yamamoto, Mayu Oura, Hiroshi Tatano, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Investigation of Amino Acid and Fatty Acid Profiles of Japanese Diets Using the Food Exchange Lists for Diabetes Diet., Journal of Nutritional Science and Vitaminology, Vol.70, No.1, 25-35, 2024. (要約) Dietary Reference Intakes for Japanese provide target values for proteins, fats, and carbohydrates. However, they do not provide information on reference values for amino acids (AAs) and fatty acids (FAs), which determine the quality of foods in detail. Therefore, we evaluated AAs and FAs using the Food Exchange Lists-Dietary Guidance for Persons with Diabetes (in Japanese) Utilization, Second Edition Sample Menus and Practice (FELD) as an ideal Japanese diet. Based on FELD, 15 different daily meal patterns were employed with combinations of three levels of carbohydrates %energy (high carbohydrate [HC], 60%; middle carbohydrate [MC], 55%; and low carbohydrate [LC], 50%) and five levels of energy (1,200-2,000 kcal). Using the Japanese Food Composition Table 2020 adjusted for 1,000 kcal, 18 AAs, 49 FAs, and calorie densities (CDs, kcal/g) were calculated and compared among the three groups. Dietary AA was rich in glutamic acid, aspartic acid, and leucine; in order, no significant differences were observed among HC, MC, and LC for 18 AAs. Dietary FA was higher for 18:1 total, 16:0, and 18:2 n-6. Moreover, 16:0, 20:0, and 18:1 total in LC and 22:0 and 18:3 n-3 in MC were significantly higher than those in HC. The HC, MC, and LC CD was low at 0.82, 0.84, and 0.93 kcal/g, respectively. No significant differences in 18 AAs and CD were noted among HC, MC, and LC in FELD; however, significant differences were observed in the FA profiles. This study suggests the importance of evaluating diet using AA and FA units. (キーワード) Fatty Acids / Amino Acids / Dietary Carbohydrates / Diet / Dietary Fats / 糖尿病 (diabetes mellitus) (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.70.25 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38417849 ● CiNii @ 国立情報学研究所 (CRID): 1390017843874880896 ● Summary page in Scopus @ Elsevier: 2-s2.0-85186634749 (DOI: 10.3177/jnsv.70.25, PubMed: 38417849, CiNii: 1390017843874880896, Elsevier: Scopus)
5.	Ayari Tsumura, Hisami Yamanaka-Okumura, Hana Kawakami, Shiori Yamamoto, Mayu Oura, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Amino acid and fatty acid profiles of the average Japanese diet: Fusion of the National Health and Nutrition Examination Survey and the Food Composition Database, Human Nutrition and Metabolism, Vol.33, 200200, 2023. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.hnm.2023.200200 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1360863416724271488 ● Summary page in Scopus @ Elsevier: 2-s2.0-85162872341 (DOI: 10.1016/j.hnm.2023.200200, CiNii: 1360863416724271488, Elsevier: Scopus)
6.	Naoko Oda, Kohei Sugihara, Takashi Uebanso, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., Journal of Clinical Biochemistry and Nutrition, Vol.73, No.3, 221-227, 2023. (要約) were observed in high phosphate diet group. Furthermore, high phosphate diet induced reduction of microbial diversity and decreased mRNA levels of colonic tight junction markers. These results suggest that the excessive intake of dietary phosphate disturbs gut microbiota and affects intestinal barrier function. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.23-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970557 ● Search Scopus @ Elsevier (PMID): 37970557 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-9 (DOI: 10.3164/jcbn.23-9, PubMed: 37970557)
7.	Yuki Kamei, Yosuke Okumura, Yuichiro Adachi, Yuki Mori, Maiko Sakai, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Humoral and cellular factors inhibit phosphate-induced vascular calcification during the growth period., Journal of Clinical Biochemistry and Nutrition, Vol.73, No.3, 198-204, 2023. (要約) , obvious calcification was observed in the adult aorta but not in the young aorta. Furthermore, culture in high Pi medium increased the mRNA level of tissue-nonspecific alkaline phosphatase (TNAP), which degrades pyrophosphate, only in the adult aorta. Collectively, our findings indicate that the aorta in growing mouse may be resistant to Pi-induced vascular calcification via a mechanism in which high serum fetuin-A levels and suppressed TNAP expression. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.23-11 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970550 ● Search Scopus @ Elsevier (PMID): 37970550 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-11 (DOI: 10.3164/jcbn.23-11, PubMed: 37970550)
8.	Yilimulati Yimamu, Ayako Ohtani, Yuichiro Takei, Airi Furuichi, Yuki Kamei, Hisami Okumura, Hirokazu Ohminami, Masashi Masuda, Makoto Miyazaki, Hironori Yamamoto and Yutaka Taketani : 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) induces ectopic calcification., Journal of Clinical Biochemistry and Nutrition, Vol.71, No.2, 103-111, 2022. (要約) Vascular calcification is an important pathogenesis related to cardiovascular disease and high mortality rate in chronic kidney disease (CKD) patients. It has been well-known that hyper-phosphatemia induces osteochondrogenic transition of vascular smooth muscle cells (VSMCs) resulting ectopic calcification in aortic media, cardiac valve, and kidney. However, the detailed mechanism of the ectopic calcification has been not clarified yet. Here, we found that the co-localization of CYP27B1 with the calcified lesions of aorta and arteries in kidney of klotho mutant () mice, and then investigated the role of CYP27B1 in the mineralization of the VSMCs. Under high phosphate condition, overexpression of CYP27B1 induced calcification and osteocalcin mRNA expression in the VSMCs. Inversely, siRNA- inhibited high phosphate-induced calcification of the VSMCs. We also found that the accumulated CYP27B1 protein was glycosylated in the kidney of mice. Therefore, overexpression of CYP27B1-N310A and CYP27B1-T439A, which are a mutation for -linked glycosylation site (N310A) and a mutation for -linked glycosylation site (T439A) in CYP27B1, decreased calcium deposition and expression of RUNX2 induced by high phosphate medium in VSMCs compared with wild-type CYP27B1. These results suggest that extra-renal expression of glycosylated CYP27B1 would be required for ectopic calcification of VSMCs under hyperphosphatemia. (徳島大学機関リポジトリ) ● Metadata: 117147 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.22-16 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36213783 ● Search Scopus @ Elsevier (PMID): 36213783 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.22-16 (徳島大学機関リポジトリ: 117147, DOI: 10.3164/jcbn.22-16, PubMed: 36213783)
9.	Masashi Masuda, Risa Yoshida-Shimizu, Yuki Mori, Kohta Ohnishi, Yuichiro Adachi, Maiko Sakai, Serina Kabutoya, Hirokazu Ohminami, Hirokazu Ohminami, Hironori Yamamoto, Makoto Miyazaki and Yutaka Taketani : Sulforaphane induces lipophagy through the activation of AMPK-mTOR-ULK1 pathway signaling in adipocytes., The Journal of Nutritional Biochemistry, Vol.106, 109017, 2022. (要約) Lipophagy, a form of selective autophagy, degrades lipid droplet (LD) in adipose tissue and the liver. The chemotherapeutic isothiocyanate sulforaphane (SFN) contributes to lipolysis through the activation of hormone-sensitive lipase and the browning of white adipocytes. However, the details concerning the regulation of lipolysis in adipocytes by SFN-mediated autophagy remain unclear. In this study, we investigated the effects of SFN on autophagy in the epididymal fat of mice fed a high-fat diet (HFD) or control-fat diet and on the molecular mechanisms of autophagy in differentiated 3T3-L1 cells. Western blotting revealed that the protein expression of lipidated LC3 (LC3-II), an autophagic substrate, was induced after 3T3-L1 adipocytes treatment with SFN. In addition, SFN increased the LC3-II protein expression in the epididymal fat of mice fed an HFD. Immunofluorescence showed that the SFN-induced LC3 expression was co-localized with LDs in 3T3-L1 adipocytes and with perilipin, the most abundant adipocyte-specific protein, in adipocytes of mice fed an HFD. Next, we confirmed that SFN activates autophagy flux in differentiated 3T3-L1 cells using the mCherry-EGFP-LC3 and GFP-LC3-RFP-LC3 probe. Furthermore, we examined the induction mechanisms of autophagy by SFN in 3T3-L1 adipocytes using western blotting. ATG5 knockdown partially blocked the SFN-induced release of fatty acids from LDs in mature 3T3-L1 adipocytes. SFN time-dependently elicited the phosphorylation of AMPK, the dephosphorylation of mTOR, and the phosphorylation of ULK1 in differentiated 3T3-L1 cells. Taken together, these results suggest that SFN may provoke lipophagy through AMPK-mTOR-ULK1 pathway signaling, resulting in partial lipolysis of adipocytes. (キーワード) 3T3-L1 Cells / AMP-Activated Protein Kinases / Adipocytes, White / Animals / オートファジー (autophagy) / Autophagy-Related Protein-1 Homolog / Isothiocyanates / Lipolysis / Mice / シグナル伝達 (signal transduction) / Sulfoxides / TOR Serine-Threonine Kinases (徳島大学機関リポジトリ) ● Metadata: 117431 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2022.109017 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35461903 ● Search Scopus @ Elsevier (PMID): 35461903 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2022.109017 (徳島大学機関リポジトリ: 117431, DOI: 10.1016/j.jnutbio.2022.109017, PubMed: 35461903)
10.	Yuichiro Adachi, Masashi Masuda, Iori Sakakibara, Takayuki Uchida, Yuki Niida, Yuki Mori, Yuki Kamei, Yosuke Okumura, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Takeshi Nikawa and Yutaka Taketani : All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal., Life Science Alliance, Vol.5, No.7, 2022. (要約) All-trans retinoic acid (ATRA) increases the sensitivity to unfolded protein response in differentiating leukemic blasts. The downstream transcriptional factor of PERK, a major arm of unfolded protein response, regulates muscle differentiation. However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. In this study, we identified ATRA increased the GADD34 expression independent of the PERK signal in the gastrocnemius muscle of mice. ATRA up-regulated GADD34 expression through the transcriptional activation of gene via inhibiting the interaction of homeobox Six1 and transcription co-repressor TLE3 with the MEF3-binding site on the gene promoter in skeletal muscle. ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on mRNA via p-38 MAPK, resulting in the instability of mRNA. Overexpressed GADD34 in C2C12 cells changes the type of myosin heavy chain in myotubes. These results suggest ATRA increases GADD34 expression via transcriptional and post-transcriptional regulation, which changes muscle fiber type. (キーワード) Animals / Gene Expression Regulation / MAP Kinase Signaling System / Mice / Muscle Fibers, Skeletal / Protein Phosphatase 1 / RNA, Messenger / Transcription Factors / Tretinoin (徳島大学機関リポジトリ) ● Metadata: 117429 (出版サイトへのリンク) ● Publication site (DOI): 10.26508/lsa.202101345 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35318262 ● Search Scopus @ Elsevier (PMID): 35318262 ● Search Scopus @ Elsevier (DOI): 10.26508/lsa.202101345 (徳島大学機関リポジトリ: 117429, DOI: 10.26508/lsa.202101345, PubMed: 35318262)
11.	Kiyoshi Tanaka, Yutaka Taketani, Imelda Angeles-Agdeppa and Taiho Kambe : Role of vitamins and minerals in health and diseases, Journal of Nutritional Science and Vitaminology, Vol.68, No.S70-S72, S70-S72, 2022. (要約) We have adopted the following four topics: 1) dietary phosphorus management in chronic kidney disease (CKD) patients, 2) inadequate nutrient intakes in Filipino schoolchildren and adolescents, 3) clinical and societal implications of vitamin insufficiency, and 4) zinc transporters. Vitamins and minerals play essential roles in health promotion in clinical and societal perspectives with marked advances in understanding the mechanism underlying such effects. (キーワード) Adolescent / Humans / Child / Vitamins / Vitamin A / Minerals / Vitamin K / Phosphorus (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.68.S70 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36437023 ● CiNii @ 国立情報学研究所 (CRID): 1390575683445630976 ● Summary page in Scopus @ Elsevier: 2-s2.0-85142826644 (DOI: 10.3177/jnsv.68.S70, PubMed: 36437023, CiNii: 1390575683445630976, Elsevier: Scopus)
12.	Shinta Nishioka, Hidetaka Wakabayashi, Jun Kayashita, Yutaka Taketani and Ryo Momosaki : Predictive validity of the Mini Nutritional Assessment Short-Form for rehabilitation patients: A retrospective analysis of the Japan Rehabilitation Nutrition Database., Journal of Human Nutrition and Dietetics, 2021. (要約) Malnutrition is associated with worse outcome in rehabilitation patients; however, appropriate malnutrition screening tools for this population have not been investigated. We examined the predictive validity of specific cut-off values of the Mini Nutritional Assessment Short-Form version 2 (MNA-SFv2) for Japanese rehabilitation patients. This retrospective cohort study analyzed adult patients (≥ 20 years) in the Japan Rehabilitation Nutrition Database who were in convalescent rehabilitation wards after stroke or hip fracture. Patients were classified into three categories based on MNA-SFv2 original (0-7, 8-11 and 12-14 points, respectively) or modified (0-5, 6-7 and 8-14 points, respectively) cut-off values: malnutrition, at risk of malnutrition or well-nourished. Functional independence measure (FIM) and home discharge were compared between the categories. Overall, 489 patients were analyzed. Based on the MNA-SFv2 original and modified cut-off values, 64.4% and 36.0% were malnourished, 32.3% and 28.4% were at risk of malnutrition, and 3.3% and 35.6% were well-nourished, respectively. Malnutrition defined by both cut-off values was significantly associated with the FIM at admission, whereas only those defined by modified cut-off values predicted the FIM at discharge (B, -7.1; 95% confidence interval = -12.3 to -1.9). Neither original, nor modified cut-off values predicted discharge to home and long-term care facilities. An MNA-SFv2 score of 0-5 points may be useful to identify Japanese patients with poor outcomes in a rehabilitation setting. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jhn.12887 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33713369 ● Search Scopus @ Elsevier (PMID): 33713369 ● Search Scopus @ Elsevier (DOI): 10.1111/jhn.12887 (DOI: 10.1111/jhn.12887, PubMed: 33713369)
13.	Kohta Ohnishi, Yano Satoshi, Fujimoto Moe, Sakai Maiko, Harumoto Erika, Furuichi Airi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Hara Taichi and Yutaka Taketani : Identification of Dietary Phytochemicals Capable of Enhancing the Autophagy Flux in HeLa and Caco-2 Human Cell Lines, Antioxidants, Vol.9, No.12, E1193, 2020. (キーワード) オートファジー (autophagy) / 植物性食品成分 / 構造活性相関 (structureactivity relationship) (徳島大学機関リポジトリ) ● Metadata: 115876 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/antiox9121193 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85096821054 (徳島大学機関リポジトリ: 115876, DOI: 10.3390/antiox9121193, Elsevier: Scopus)
14.	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. (徳島大学機関リポジトリ) ● Metadata: 114726 (出版サイトへのリンク) ● Publication site (DOI): 10.1053/j.jrn.2020.02.005 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114726, DOI: 10.1053/j.jrn.2020.02.005, PubMed: 32778471)
15.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114417 (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BCJ20190716 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357 ● Search Scopus @ Elsevier (PMID): 32016357 ● Search Scopus @ Elsevier (DOI): 10.1042/BCJ20190716 (徳島大学機関リポジトリ: 114417, DOI: 10.1042/BCJ20190716, PubMed: 32016357)
16.	Maiko Sakai, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Taichi Hara and Yutaka Taketani : Isorhamnetin, a 3'-methoxylated flavonol, enhances the lysosomal proteolysis in J774.1 murine macrophages in a TFEB-independent manner., Bioscience, Biotechnology, and Biochemistry, 2020. (要約) Lysosome is the principal organelle for the ultimate degradation of cellular macromolecules, which are delivered through endocytosis, phagocytosis, and autophagy. The lysosomal functions have been found to be impaired by fatty foods and aging, and more importantly, the lysosomal dysfunction in macrophages has been reported as a risk of atherosclerosis development. In this study, we searched for dietary polyphenols which possess the activity for enhancing the lysosomal degradation in J774.1, a murine macrophage-like cell line. Screening test utilizing DQ-BSA digestion identified isorhamnetin (3'--methylquercetin) as an active compound. Interestingly, structural comparison to inactive flavonols revealed that the chemical structure of the B-ring moiety in isorhamnetin is the primary determinant of its lysosome-enhancing activity. Unexpectedly isorhamnetin failed to inhibit mTORC1-TFEB signaling, a master regulator of lysosomal biogenesis and function. Our data suggested that the other molecular mechanism might be critical for the regulation of lysosomes in macrophages. ANOVA: analysis of variance; ApoE: apolipoprotein E; ATP6V0D2: ATPase H transporting V0 subunit d2; BAF: bafilomycin A1; BODIPY: boron dipyrromethene; BSA: bovine serum albumin; CTSD: cathepsin D; CTSF: cathepsin F; DMEM: Dulbecco's modified eagle medium; DMSO: dimethyl sulfoxide; EGCG: epigallocatechin-3-gallate; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HPLC: high-performance liquid chromatography; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LC-MS/MS: liquid chromatography tandem mass spectrometry; MITF: microphthalmia-associated transcription factor; MRM: multiple reaction monitoring; mTORC1: mechanistic target of rapamycin complex 1; PBS: phosphate-buffered saline; PPARγ: peroxisome proliferator-activated receptor γ; RT-qPCR: reverse transcription quantitative polymerase chain reaction; SDS: sodium dodecyl sulfate; SNARE: soluble N-ethylmaleimide-sensitive-factor attachment protein receptor; TBS: Tris-buffered saline; TFA: trifluoroacetic acid; TFE3: transcription factor binding to IGHM enhancer 3; TFEB: transcriptional factor EB; TFEC: transcription factor EC; V-ATPase: vacuolar-type proton ATPase. (キーワード) イソラムネチン / TFEB / リソソーム / マクロファージ (macrophage) / ポリフェノール (polyphenol) (徳島大学機関リポジトリ) ● Metadata: 116062 (出版サイトへのリンク) ● Publication site (DOI): 10.1080/09168451.2020.1727309 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32046625 ● Summary page in Scopus @ Elsevier: 2-s2.0-85079428723 (徳島大学機関リポジトリ: 116062, DOI: 10.1080/09168451.2020.1727309, PubMed: 32046625, Elsevier: Scopus)
17.	Yuki Niida, Masashi Masuda, Yuichiro Adachi, Aika Yoshizawa, Hirokazu Ohminami, Yuki Mori, Kohta Ohnishi, Hisami Okumura, Takayuki Uchida, Takeshi Nikawa, Hironori Yamamoto, Makoto Miyazaki and Yutaka Taketani : Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease, Journal of Clinical Biochemistry and Nutrition, Vol.67, No.2, 179-187, 2020. (要約) <p>Skeletal muscle atrophy is associated with mortality and poor prognosis in patients with chronic kidney disease (CKD). However, underlying mechanism by which CKD causes muscle atrophy has not been completely understood. The quality of lipids (lipoquality), which is defined as the functional features of diverse lipid species, has recently been recognized as the pathology of various diseases. In this study, we investigated the roles of the stearoyl-CoA desaturase (SCD), which catalyzes the conversion of saturated fatty acids into monounsaturated fatty acids, in skeletal muscle on muscle atrophy in CKD model animals. In comparison to control rats, CKD rats decreased the SCD activity and its gene expression in atrophic gastrocnemius muscle. Next, oleic acid blocked the reduction of the thickness of C2C12 myotubes and the increase of the endoplasmic reticulum stress induced by SCD inhibitor. Furthermore, endoplasmic reticulum stress inhibitor ameliorated CKD-induced muscle atrophy (the weakness of grip strength and the decrease of muscle fiber size of gastrocnemius muscle) in mice and the reduction of the thickness of C2C12 myotubes by SCD inhibitor. These results suggest that the repression of SCD activity causes muscle atrophy through excessive endoplasmic reticulum stress in CKD.</p> (キーワード) skeletal muscle atrophy / endoplasmic reticulum stress / chronic kidney disease / stearoyl-CoA desaturase / saturated fatty acid (徳島大学機関リポジトリ) ● Metadata: 114720 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.20-24 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33041516 ● CiNii @ 国立情報学研究所 (CRID): 1390566775163696384 ● Search Scopus @ Elsevier (PMID): 33041516 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.20-24 (徳島大学機関リポジトリ: 114720, DOI: 10.3164/jcbn.20-24, PubMed: 33041516, CiNii: 1390566775163696384)
18.	Keisuke Kawamoto, Masae Sakuma, Sarasa Tanaka, Masashi Masuda, Mari Nakao-Muraoka, Yuki Niida, Yurino Nakamatsu, Mikiko Ito, Yutaka Taketani and Hidekazu Arai : High-fat diets provoke phosphorus absorption from the small intestine in rats., Nutrition, Vol.72, 2019. (徳島大学機関リポジトリ) ● Metadata: 114416 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.nut.2019.110694 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32007805 ● Search Scopus @ Elsevier (PMID): 32007805 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nut.2019.110694 (徳島大学機関リポジトリ: 114416, DOI: 10.1016/j.nut.2019.110694, PubMed: 32007805)
19.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114242 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.19-79 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114242, DOI: 10.3164/jcbn.19-79, PubMed: 32001956)
20.	Shiori Fukuda-Tatano, Hironori Yamamoto, Otoki Nakahashi, Ryouhei Yoshikawa, Mayu Hayashi, Maki Kishimoto, Yukiko Imi, Hisami Okumura, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Regulation of α-Klotho Expression by Dietary Phosphate During Growth Periods., Calcified Tissue International, Vol.104, No.6, 667-678, 2019. (要約) Inorganic phosphate (Pi) is an essential nutrient for maintaining various biological functions, particularly during growth periods. Excess intake of dietary Pi increases the secretion of fibroblast growth factor 23 (FGF23) and parathyroid hormone to maintain plasma Pi levels. FGF23 is a potent phosphaturic factor that binds to the α-klotho/FGFR complex in the kidney to promote excretion of Pi into the urine. In addition, excess intake of dietary Pi decreases renal α-klotho expression. Down-regulation or lack of α-klotho induces a premature aging-like phenotype, resulting from hyperphosphatemia, and leading to conditions such as ectopic calcification and osteoporosis. However, it remains unclear what effects dietary Pi has on α-klotho expression at different life stages, especially during growth periods. To investigate this, we used C57BL/6J mice in two life stages during growing period. Weaned (3 weeks old) and periadolescent (7 weeks old) were randomly divided into seven experimental groups and fed with 0.02, 0.3, 0.6, 0.9, 1.2, 1.5, or 1.8% Pi diets for 7 days. As a result, elevated plasma Pi and FGF23 levels and decreased renal α-klotho expression were observed in weaned mice fed with a high Pi diet. In addition, a high Pi diet clearly induced renal calcification in the weaned mice. However, in the periadolescent group, renal calcification was not observed, even in the 1.8% Pi diet group. The present study indicates that a high Pi diet in weaned mice has much greater adverse effects on renal α-klotho expression and pathogenesis of renal calcification compared with periadolescent mice. (徳島大学機関リポジトリ) ● Metadata: 113367 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00223-019-00525-0 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30671592 ● Search Scopus @ Elsevier (PMID): 30671592 ● Search Scopus @ Elsevier (DOI): 10.1007/s00223-019-00525-0 (徳島大学機関リポジトリ: 113367, DOI: 10.1007/s00223-019-00525-0, PubMed: 30671592)
21.	Yukiko Imi, Norie Yabiki, Maerjianghan Abuduli, Masashi Masuda, Hisami Okumura and Yutaka Taketani : High phosphate diet suppresses lipogenesis in white adipose tissue., Journal of Clinical Biochemistry and Nutrition, Vol.63, No.3, 181-191, 2018. (要約) Excessive phosphate intake has been positively associated with renal and vascular dysfunction, conversely negatively associated with body fat accumulation. We investigated the effect of a high-phosphate diet on the expression of lipid metabolic genes in white adipose tissue and liver. Male 8-week-old Sprague-Dawley rats were fed a control diet containing 0.6% phosphate or a high-phosphate diet containing 1.5% phosphate for 4 weeks. In comparison to the control group, the HP group showed a significantly lower body fat mass and fasting plasma insulin level alongside decreased lipogenic and increased lipolytic gene expression in visceral fat. Additionally, the expression of genes involved in hepatic lipogenesis, hepatic glycogenesis, and triglyceride accumulation decreased in the high-phosphate group. Exogenous phosphate, parathyroid hormone, and fibroblast growth factor 23 did not directly affect the expression of lipolytic or lipogenic genes in 3T3-L1 adipocytes and HepG2 hepatocytes. Thus, the high-phosphate diet suppressed the activity of white adipose tissue by increasing lipolytic gene expression and decreasing lipogenic gene expression. These effects could have been caused by the lowered fasting plasma insulin level that occurred in response to the high-phosphate diet, but were not directly caused by the increases in plasma phosphate or phosphaturic hormones. (徳島大学機関リポジトリ) ● Metadata: 111624 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.17-141 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30487667 ● Search Scopus @ Elsevier (PMID): 30487667 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.17-141 (徳島大学機関リポジトリ: 111624, DOI: 10.3164/jcbn.17-141, PubMed: 30487667)
22.	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. (要約) ) 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. (徳島大学機関リポジトリ) ● Metadata: 112883 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2018.04.058 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 112883, DOI: 10.1016/j.bbrc.2018.04.058, PubMed: 29653103)
23.	Chise Yamaguchi, Hisami Okumura, Haruka Esumi, Masashi Masuda, Takafumi Katayama and Yutaka Taketani : Investigation of dose-dependent effects of fat on blood glucose, serum insulin, and appetite sensation., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 203-207, 2018. (要約) , respectively. We conducted a randomized, crossover trial and measured laboratory data and appetite sensation via the visual analog scale. Each participant was provided with four different test meals. They consisted of common, basic foods and contained 75 g liquid glucose and 4 slices of crackers to which 0 g butter (control), 10 g butter (B10), 20 g butter (B20), and 40 g butter (B40) were added, respectively. The results indicated that single ingestion of butter did not influence laboratory values of glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), total bile acids, or high-sensitivity CRP (hs-CRP). Regarding postprandial appetite sensation, appetite ratings for fullness were the highest after the B40 meal (p < 0.05);however, satisfaction ratings were not significantly different after the ingestion of this meal. Ratings were significantly different after the B20 meal. In conclusion, healthy adult subjects experienced fullness and satisfaction after ingesting 20-40 g of butter. J. Med. Invest. 65:203-207, August, 2018. (キーワード) Adult / Appetite / Blood Glucose / Cross-Over Studies / Dietary Fats / Dose-Response Relationship, Drug / Female / Humans / Insulin / Male / Postprandial Period (徳島大学機関リポジトリ) ● Metadata: 112238 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.65.203 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282861 ● Search Scopus @ Elsevier (PMID): 30282861 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.203 (徳島大学機関リポジトリ: 112238, DOI: 10.2152/jmi.65.203, PubMed: 30282861)
24.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 111009 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.17-20 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111009, DOI: 10.3164/jcbn.17-20, PubMed: 29371756)
25.	Nagakatsu Harada, Maiko Okuyama, Aya Yoshikatsu, Hironori Yamamoto, Saori Ishiwata, Chikako Hamada, Tomoyo Hirose, Masayuki Shono, Masashi Kuroda, Rie Tsutsumi, Jiro Takeo, Yutaka Taketani, Yutaka Nakaya and Hiroshi Sakaue : Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism., Journal of Cellular Biochemistry, Vol.118, No.11, 3810-3824, 2017. (出版サイトへのリンク) ● Publication site (DOI): 10.1002/jcb.26031 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28383761 ● Search Scopus @ Elsevier (PMID): 28383761 ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.26031 (DOI: 10.1002/jcb.26031, PubMed: 28383761)
26.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 110124 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.16-117 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 110124, DOI: 10.3164/jcbn.16-117, PubMed: 28955125)
27.	Naoko Takase, Masatoshi Inden, Shin-Ichiro Sekine, Yumi Ishii, Hiroko Yonemitsu, Wakana Iwashita, Hisaka Kurita, Yutaka Taketani and Isao Hozumi : Neuroprotective effect of 5-aminolevulinic acid against low inorganic phosphate in neuroblastoma SH-SY5Y cells., Scientific Reports, Vol.7, No.1, 2017. (要約) PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2) are type-III sodium-dependent phosphate cotransporters (NaPiTs). Recently, SLC20A2 mutations have been found in patients with idiopathic basal ganglia calcification (IBGC), and were predicted to bring about an inability to transport Pi from the extracellular environment. Here we investigated the effect of low Pi loading on the human neuroblastoma SH-SY5Y and the human glioblastoma A172 cell lines. The results show a different sensitivity to low Pi loading and differential regulation of type-III NaPiTs in these cells. We also examined whether 5-aminolevulinic acid (5-ALA) inhibited low Pi loading-induced neurotoxicity in SH-SY5Y cells. Concomitant application of 5-ALA with low Pi loading markedly attenuated low Pi-induced cell death and mitochondrial dysfunction via the induction of HO-1 by p38 MAPK. The findings provide us with novel viewpoints to understand the pathophysiology of IBGC, and give a new insight into the clinical prevention and treatment of IBGC. (徳島大学機関リポジトリ) ● Metadata: 112434 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-017-06406-6 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28720798 ● Search Scopus @ Elsevier (PMID): 28720798 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-06406-6 (徳島大学機関リポジトリ: 112434, DOI: 10.1038/s41598-017-06406-6, PubMed: 28720798)
28.	A Takashima, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, S Nishimoto, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yutaka Taketani, Michio Shimabukuro and Masataka Sata : Combination of n-3 polyunsaturated fatty acids reduces atherogenesis in apolipoprotein E-deficient mice by inhibiting macrophage activation., Atherosclerosis, Vol.254, 142-150, 2016. (要約) BACKGROUND AND AIMS: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are major components of n-3 polyunsaturated fatty acids (n-3 PUFAs) which inhibit atherogenesis, although few studies have examined the effects of the combination of EPA and DHA on atherogenesis. The aim of this study was to investigate whether DHA has additional anti-atherosclerotic effects when combined with EPA.METHODS: Male 8-week-old apolipoprotein E-deficient (Apoe-/-) mice were fed a western-type diet supplemented with different amounts of EPA and DHA; EPA (2.5%, w/w), low-dose EPA + DHA (2.5%, w/w), or high-dose EPA + DHA (5%, w/w) for 20 weeks. The control group was fed a western-type diet containing no n-3 PUFA. Histological and gene expression analysis were performed in atherosclerotic lesions in the aorta. To address the mechanisms, RAW264.7 cells were used.RESULTS: All n-3 PUFA treatments significantly attenuated the development and destabilization of atherosclerotic plaques compared with the control. The anti-atherosclerotic effects were enhanced in the high-dose EPA + DHA group (p < 0.001), whereas the pure EPA group and low-dose EPA + DHA group showed similar results. EPA and DHA additively attenuated the expression of inflammatory molecules in RAW264.7 cells stimulated with LPS. DHA or EPA + DHA suppressed LPS-induced toll-like receptor 4 (TLR4) expression in lipid rafts on RAW264.7 cells (p < 0.05). Lipid raft disruption by methyl--cyclodextrin suppressed mRNA expression of inflammatory molecules in LPS-stimulated macrophages.CONCLUSION: n-3 PUFAs suppressed atherogenesis. DHA combined with EPA had additional anti-inflammatory effects and inhibited atherogenesis in Apoe-/- mice. The reduction of TLR4 expression in lipid rafts in macrophages by DHA might be involved in this mechanism, at least partially. (キーワード) Atherosclerosis / Inflammation / Lipid raft / Macrophage / Toll-like receptor 4 / n-3 poly unsaturated fatty acid (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2016.10.002 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27744130 ● Summary page in Scopus @ Elsevier: 2-s2.0-84991678518 (DOI: 10.1016/j.atherosclerosis.2016.10.002, PubMed: 27744130, Elsevier: Scopus)
29.	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. (要約) 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. (キーワード) Adult / Cross-Over Studies / Diet, High-Fat / Dietary Fats / Energy Intake / Female / Humans / Meals / Satiation / Vegetables / Young Adult (徳島大学機関リポジトリ) ● Metadata: 109710 (出版サイトへのリンク) ● Publication site (DOI): 10.6133/apjcn.092015.25 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27440681 ● Summary page in Scopus @ Elsevier: 2-s2.0-84989767515 (徳島大学機関リポジトリ: 109710, DOI: 10.6133/apjcn.092015.25, PubMed: 27440681, Elsevier: Scopus)
30.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 109976 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpendo.00234.2015 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 109976, DOI: 10.1152/ajpendo.00234.2015, PubMed: 26786774)
31.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 109711 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.nutres.2015.09.001 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 109711, DOI: 10.1016/j.nutres.2015.09.001, PubMed: 26475181)
32.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.14-132 (文献検索サイトへのリンク) ● 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)
33.	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. (要約) This study indicates that the FO, which is a rich source of ALA, leads to lower sd-LDL cholesterol concentrations. (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s12937-015-0023-2 (文献検索サイトへのリンク) ● 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)
34.	Toshinori Chiba, Hirotaka Matsuo, Yusuke Kawamura, Shushi Nagamori, Takashi Nishiyama, Ling Wei, Akiyoshi Nakayama, Takahiro Nakamura, Masayuki Sakiyama, Tappei Takada, Yutaka Taketani, Shino Suma, Mariko Naito, Takashi Oda, Hiroo Kumagai, Yoshinori Moriyama, Kimiyoshi Ichida, Toru Shimizu, Yoshikatsu Kanai and Nariyoshi Shinomiya : NPT1/SLC17A1 is a renal urate exporter in humans and its common gain-of-function variant decreases the risk of renal underexcretion gout., Arthritis & Rheumatology, Vol.67, No.1, 281-287, 2015. (要約) This study showed that NPT1 is a urate exporter located in the renal proximal tubule in humans, and that its common gain-of-function variant, rs1165196, causes RUE gout, a major subtype of gout. These findings enable us to deepen our understanding of the physiologic role of NPT1 as a renal urate exporter as well as its pathophysiologic role in gout. (キーワード) Amino Acid Sequence / Animals / Case-Control Studies / Female / Gene Frequency / Genetic Predisposition to Disease / Genotype / Gout / Humans / Kidney / Kidney Tubules, Proximal / Male / Molecular Sequence Data / Mutation, Missense / Oocytes / Polymorphism, Single Nucleotide / Risk Factors / Sodium-Phosphate Cotransporter Proteins, Type I / Uric Acid / Xenopus (出版サイトへのリンク) ● Publication site (DOI): 10.1002/art.38884 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25252215 ● Summary page in Scopus @ Elsevier: 2-s2.0-84919926008 (DOI: 10.1002/art.38884, PubMed: 25252215, Elsevier: Scopus)
35.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.61.S173 (文献検索サイトへのリンク) ● 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)
36.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 106333 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.14-96 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 106333, DOI: 10.3164/jcbn.14-96, PubMed: 25678749)
37.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 106169 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.14-11 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 106169, DOI: 10.3164/jcbn.14-11, PubMed: 25147427)
38.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.14-15 (文献検索サイトへのリンク) ● 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)
39.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 106159 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.13-109 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 106159, DOI: 10.3164/jcbn.13-109, PubMed: 24688219)
40.	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. (要約) 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. (キーワード) 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 (徳島大学機関リポジトリ) ● Metadata: 106168 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00474.2013 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 106168, DOI: 10.1152/ajprenal.00474.2013, PubMed: 24500689)
41.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3945/an.113.004002 (文献検索サイトへのリンク) ● 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)
42.	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. (要約) 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. (キーワード) transporter / nutrient homeostasis / polymorphism / lifestyle-related disease (出版サイトへのリンク) ● Publication site (DOI): 10.7600/jpfsm.2.409 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205415412992 ● Search Scopus @ Elsevier (DOI): 10.7600/jpfsm.2.409 (DOI: 10.7600/jpfsm.2.409, CiNii: 1390001205415412992)
43.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 105925 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.13-48 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 105925, DOI: 10.3164/jcbn.13-48, PubMed: 24249969)
44.	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. (要約) Gene expression profiling in the WBC can reflect food-related metabolic changes, even in the postprandial state. (キーワード) Blood Glucose / Cross-Over Studies / Gene Expression Profiling / Glycemic Index / Humans / Insulin / Leukocytes / Male / Oligonucleotide Array Sequence Analysis / Transcriptome (徳島大学機関リポジトリ) ● Metadata: 109379 (出版サイトへのリンク) ● Publication site (DOI): 10.1159/000354247 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24008923 ● Search Scopus @ Elsevier (PMID): 24008923 ● Search Scopus @ Elsevier (DOI): 10.1159/000354247 (徳島大学機関リポジトリ: 109379, DOI: 10.1159/000354247, PubMed: 24008923)
45.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.nutres.2013.05.004 (文献検索サイトへのリンク) ● 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)
46.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2012-1647 (文献検索サイトへのリンク) ● 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)
47.	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. (要約) 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. (キーワード) Animals / コレステロール (cholesterol) / Cholesterol, Dietary / Female / Hypercholesterolemia / Lipids / Liver / Male / Mice / ノックアウトマウス (knockout mice) / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa (徳島大学機関リポジトリ) ● Metadata: 106356 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.60.191 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24190035 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887001043 (徳島大学機関リポジトリ: 106356, DOI: 10.2152/jmi.60.191, PubMed: 24190035, Elsevier: Scopus)
48.	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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bone.2012.07.006 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-84865661013 (DOI: 10.1016/j.bone.2012.07.006, Elsevier: Scopus)
49.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1017/S0007114511004156 (文献検索サイトへのリンク) ● 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)
50.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2011.03.023 (文献検索サイトへのリンク) ● 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)
51.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.10-150 (文献検索サイトへのリンク) ● 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)
52.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0022976 (文献検索サイトへのリンク) ● 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)
53.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.10-111 (文献検索サイトへのリンク) ● 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)
54.	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. (要約) 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. (キーワード) Animals / Cell Line / Electrophoresis, Gel, Two-Dimensional / Electrophoresis, Polyacrylamide Gel / Kidney Cortex / Kidney Tubules, Proximal / LDL-Receptor Related Protein 2 / Male / Membrane Microdomains / 分子量 (molecular weight) / Multiprotein Complexes / Opossums / Protein Interaction Domains and Motifs / Rats / Rats, Sprague-Dawley / Sodium-Phosphate Cotransporter Proteins, Type IIa / Tandem Mass Spectrometry (徳島大学機関リポジトリ) ● Metadata: 82750 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.58.140 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 82750, DOI: 10.2152/jmi.58.140, PubMed: 21372499)
55.	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. (要約) 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 (キーワード) 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 / 活性酸素 (reactive oxygen species) / Soybeans / Spinacia oleracea (徳島大学機関リポジトリ) ● Metadata: 79153 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.57.314 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20847532 ● Summary page in Scopus @ Elsevier: 2-s2.0-78649650737 (徳島大学機関リポジトリ: 79153, DOI: 10.2152/jmi.57.314, PubMed: 20847532, Elsevier: Scopus)
56.	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. (要約) 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. (キーワード) Animals / COS Cells / Cercopithecus aethiops / Dogs / Electrophoretic Mobility Shift Assay / Female / Gene Expression Regulation / Hela Cells / 生体恒常性 (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 (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BJ20090671 (文献検索サイトへのリンク) ● 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)
57.	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. (要約) 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. (キーワード) Animals / Body Weight / 四塩化炭素 (carbon tetrachloride) / グルコース (glucose) / インスリン (insulin) / インスリン抵抗性 (insulin resistance) / Liver / Liver Cirrhosis, Experimental / Male / Organ Size / Rats / Rats, Sprague-Dawley (徳島大学機関リポジトリ) ● Metadata: 77532 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.57.54 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 77532, DOI: 10.2152/jmi.57.54, PubMed: 20299743)
58.	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. (要約) 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. (キーワード) Animals / Blood Glucose / Caloric Restriction / Cells, Cultured / Diet, Reducing / Dietary Proteins / Fasting / Fatty Liver / Feeding Behavior / Hypertriglyceridemia / Male / 肥満症 (obesity) / Rats / Rats, Sprague-Dawley / シグナル伝達 (signal transduction) / Sucrose (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpendo.00014.2009 (文献検索サイトへのリンク) ● 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)
59.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1681/ASN.2008101106 (文献検索サイトへのリンク) ● 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)
60.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.08-232 (文献検索サイトへのリンク) ● 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)
61.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1677/JME-08-0161 (文献検索サイトへのリンク) ● 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)
62.	Masaki Yoshida, Nagakatsu Harada, Hironori Yamamoto, Yutaka Taketani, Nagakatsu Harada, Yunjie Yin, Atsushi Hattori, Tomoe Zenitani, Sayuri Hara, Haruka Yonemoto, Aki Nakamura, Masayuki Nakano, Kazuaki Mawatari, Kiyoshi Teshigawara, Hidekazu Arai, Toshio Hosaka, Akira Takahashi, Katsuhiko Yoshimoto and Yutaka Nakaya : Identification of cis-acting promoter sequences required for expression of the glycerol-3-phosphate acyltransferase 1 gene in mice., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1791, No.1, 39-52, 2009. (要約) Glycerol-3-phosphate acyltransferase 1 (GPAT1) is a rate limiting enzyme in de novo glycerophospholipid synthesis. The murine GPAT1 promoter sequence (the "classical" sequence) was reported previously. However, the organization of this DNA sequence does not fully match the mouse genome sequences on NCBI/GenBank. Here we have identified net cis-acting promoter sequences for the mouse GPAT1 gene: promoter 1a which includes part of the classical sequence and the downstream promoter 1b. Promoter 1a facilitates transcription of two alternative GPAT1 transcript variants, GPAT1-V1 and V2, while promoter 1b produces a third transcript variant, GPAT1-V3. Upstream stimulating factor-1 (USF-1) controlled both promoters whereas sterol regulatory element-binding protein-1 (SREBP-1) exclusively regulated promoter 1a activity in vitro. Feeding increased GPAT1-V1 and V2, but not V3 mRNA levels in mouse liver. The obese condition of db/db mice did not alter the hepatic expression levels of any of the three GPAT1 variants. Feeding enhanced hepatic mRNA levels, intranuclear protein levels and promoter 1a-binding levels of SREBP-1, but not of USF-1. Thus, promoter 1a was exclusively activated by routine feeding in vivo. Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice. (キーワード) Animals / Base Sequence / Cell Line, Tumor / Gene Expression Regulation, Enzymologic / Glycerol-3-Phosphate O-Acyltransferase / Hepatocytes / Humans / Male / Mice / Mice, Obese / Promoter Regions, Genetic / RNA Interference / Sterol Regulatory Element Binding Protein 1 / Upstream Stimulatory Factors (徳島大学機関リポジトリ) ● Metadata: 113301 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbalip.2008.09.005 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18983939 ● Search Scopus @ Elsevier (PMID): 18983939 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2008.09.005 (徳島大学機関リポジトリ: 113301, DOI: 10.1016/j.bbalip.2008.09.005, PubMed: 18983939)
63.	首藤恵泉, 竹谷豊, 酒井徹, 武田英二 : 高リン血症と心血管疾患, 四国医学雑誌, Vol.64, No.3,4, 114-116, 2008年. (要約) 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. (キーワード) hyperphosphatemia / cardiovascular disease / endothelial cell / oxidative stress / vascular calcification (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050564287418501888 (CiNii: 1050564287418501888)
64.	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. (要約) 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. (キーワード) Adipocytes / Animals / アポトーシス (apoptosis) / Base Sequence / DNA Primers / Dietary Carbohydrates / Dietary Fats, Unsaturated / Disease Models, Animal / Fibrosis / Humans / Islets of Langerhans / Isomaltose / Male / Metabolic Syndrome X / 肥満症 (obesity) / Oleic Acid / Rats / Rats, Zucker / Sucrose (徳島大学機関リポジトリ) ● Metadata: 110858 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.55.183 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 110858, DOI: 10.2152/jmi.55.183, PubMed: 18797130)
65.	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. (要約) 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. (キーワード) Administration, Oral / Animals / Antioxidants / Aorta / 動脈硬化 (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 (出版サイトへのリンク) ● Publication site (DOI): 10.1021/tx8000835 (文献検索サイトへのリンク) ● 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)
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. (要約) 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. (キーワード) Adult / Area Under Curve / Blood Glucose / Cross-Over Studies / Diabetes Mellitus, Type 2 / Dietary Fiber / Female / 発酵 (fermentation) / Glycemic Index / Humans / インスリン (insulin) / 日本 (Japan) / Lipids / Male / Oryza sativa / Patient Compliance / Postprandial Period / Soy Foods / Vegetables / Young Adult (文献検索サイトへのリンク) ● 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.	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. (要約) 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. (キーワード) Animals / Blood Glucose / Enzyme Inhibitors / Hyperglycemia / Insulin / Male / Momordica charantia / Plant Preparations / Postprandial Period / Rats / Rats, Sprague-Dawley / Sucrase / alpha-Glucosidases (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.53.482 (文献検索サイトへのリンク) ● 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)
68.	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. (要約) 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. (キーワード) Aging / Animals / Diabetic Nephropathies / Glycemic Index / Humans / Kidney Failure, Chronic / Mice / Mice, Knockout / Phosphates / Phosphorus, Dietary (徳島大学機関リポジトリ) ● Metadata: 111542 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.54.359 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111542, DOI: 10.2152/jmi.54.359, PubMed: 17878688)
69.	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. (要約) 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. (キーワード) Aged / Blood Glucose / Diabetes Complications / Energy Intake / Enteral Nutrition / Glycemic Index / Humans / Liver Cirrhosis / Male (徳島大学機関リポジトリ) ● Metadata: 111545 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.54.375 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111545, DOI: 10.2152/jmi.54.375, PubMed: 17878691)
70.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1093/jn/137.8.1908 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17634263 ● CiNii @ 国立情報学研究所 (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)
71.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bone.2007.02.030 (文献検索サイトへのリンク) ● 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)
72.	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. (要約) 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. (キーワード) Animals / Blood Glucose / Fructose / Glucose / Infusions, Intravenous / Insulin / Jugular Veins / Male / Mannose / Portal Vein / Rats / Rats, Sprague-Dawley / Sympathectomy, Chemical / Time Factors / Vagotomy (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpendo.00536.2006 (文献検索サイトへのリンク) ● 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)
73.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.40.221 (文献検索サイトへのリンク) ● 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)
74.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.40.234 (文献検索サイトへのリンク) ● 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)
75.	Takeo Iwata, Noriko Mizusawa, Yutaka Taketani, Mitsuo Itakura and Katsuhiko Yoshimoto : Parafibromin tumor suppressor enhances cell growth in the cells expressing SV40 large T antigen., Oncogene, Vol.26, No.42, 6176-6183, 2007. (要約) Parafibromin (PF) is a 531-amino acid protein encoded by HRPT2, a putative tumor suppressor gene recently implicated in the autosomal-dominant hyperparathyroidism-jaw tumor familial cancer syndrome and sporadic parathyroid carcinoma. To investigate effects of PF's overexpression on cell proliferation, we performed assays in four different cell lines. The transient overexpression of PF inhibited cell growth in HEK293 and NIH3T3 cells, but enhanced cell growth in the SV40 large T antigen-expressing cell lines such as 293FT and COS7 cells. In 293FT cells, PF was found to interact with SV40 large T antigen and its overexpression promoted entry into the S phase, implying that the interaction enhanced progression through the cell cycle. The tumor suppressor protein PF acts as a positive regulator of cell growth similar to an oncoprotein in the presence of SV40 large T antigen. (キーワード) Animals / Antigens, Polyomavirus Transforming / COS Cells / Cell Line / Cell Proliferation / Cercopithecus aethiops / Fibroblasts / Humans / Mice / NIH 3T3 Cells / Simian virus 40 / Tumor Suppressor Proteins (徳島大学機関リポジトリ) ● Metadata: 109649 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/sj.onc.1210445 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17404568 ● Search Scopus @ Elsevier (PMID): 17404568 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.onc.1210445 (徳島大学機関リポジトリ: 109649, DOI: 10.1038/sj.onc.1210445, PubMed: 17404568)
76.	K Yamamoto, N Shimizu, S Obi, S Kumagaya, Yutaka Taketani, A Kamiya and J Ando : Involvement of cell-surface ATP synthase in flow-induced ATP release by vascular endothelial cells., American Journal of Physiology, Heart and Circulatory Physiology, Vol.293, No.3, H1646-53, 2007. (要約) Endothelial cells (ECs) release ATP in response to shear stress, a mechanical force generated by blood flow, and the ATP released modulates EC functions through activation of purinoceptors. The molecular mechanism of the shear stress-induced ATP release, however, has not been fully elucidated. In this study, we have demonstrated that cell surface ATP synthase is involved in shear stress-induced ATP release. Immunofluorescence staining of human pulmonary arterial ECs (HPAECs) showed that cell surface ATP synthase is distributed in lipid rafts and co-localized with caveolin-1, a marker protein of caveolae. Immunoprecipitation indicated that cell surface ATP synthase and caveolin-1 are physically associated. Measurement of the extracellular metabolism of [(3)H]ADP confirmed that cell surface ATP synthase is active in ATP generation. When exposed to shear stress, HPAECs released ATP in a dose-dependent manner, and the ATP release was markedly suppressed by the membrane-impermeable ATP synthase inhibitors angiostatin and piceatannol and by an anti-ATP synthase antibody. Depletion of plasma membrane cholesterol with methyl-beta-cyclodextrin (MbetaCD) disrupted lipid rafts and abolished co-localization of ATP synthase with caveolin-1, which resulted in a marked reduction in shear stress-induced ATP release. Pretreatment of the cells with cholesterol prevented these effects of MbetaCD. Downregulation of caveolin-1 expression by transfection of caveolin-1 siRNA also markedly suppressed ATP-releasing responses to shear stress. Neither MbetaCD, MbetaCD plus cholesterol, nor caveolin-1 siRNA had any effect on the amount of cell surface ATP synthase. These results suggest that the localization and targeting of ATP synthase to caveolae/lipid rafts is critical for shear stress-induced ATP release by HPAECs. (キーワード) Adenosine Triphosphate / Caveolin 1 / Cells, Cultured / Cholesterol / Endothelium, Vascular / Humans / Membrane Microdomains / Mitochondrial Proton-Translocating ATPases / Receptors, Purinergic / Stress, Mechanical (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpheart.01385.2006 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17545472 ● Search Scopus @ Elsevier (PMID): 17545472 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.01385.2006 (DOI: 10.1152/ajpheart.01385.2006, PubMed: 17545472)
77.	Hiroko Segawa, Setsuko Yamanaka, Akemi Onitsuka, Yuka Tomoe, Masashi Kuwahata, Mikiko Ito, Yutaka Taketani and Ken-ichi Miyamoto : Parathyroid hormone-dependent endocytosis of renal type IIc Na-Pi cotransporter., American Journal of Physiology, Renal Physiology, Vol.292, No.1, F395-F403, 2007. (要約) Hereditary hypophosphatemic rickets with hypercalciuria results from mutations of the renal type IIc Na-P(i) cotransporter gene, suggesting that the type IIc transporter plays a prominent role in renal phosphate handling. The goal of the present study was to investigate the regulation of the type IIc Na-P(i) cotransporter by parathyroid hormone (PTH). Type IIc Na-P(i) cotransporter levels were markedly increased in thyroparathyroidectomized (TPTX) rats. Four hours after administration of PTH, type IIc transporter protein levels were markedly decreased in the apical membrane fraction but recovered to baseline levels at 24 h. Immunohistochemical analyses demonstrated the presence of the type IIc transporter in the apical membrane and subapical compartments in the proximal tubular cells in TPTX animals. After administration of PTH, the intensity of immunoreactive signals in apical and subapical type IIc transporter decreased in the renal proximal tubular cells in TPTX rats. Colchicine completely blocked the internalization of the type IIc transporter. In addition, leupeptin prevented the PTH-mediated degradation of the type IIa transporter in lysosomes but had no effect on PTH-mediated degradation of the lysosomal type IIc transporter. In PTH-treated TPTX rats, the internalization of the type IIc transporter occurred after administration of PTH(1-34) (PKA and PKC activator) or PTH(3-34) (PKC activator). Thus the present study demonstrated that PTH is a major hormonal regulator of the type IIc Na-P(i) cotransporter in renal proximal tubules. (キーワード) Animals / Blotting, Northern / Cell Membrane / Endocytosis / Immunohistochemistry / Kidney / Lysosomes / Male / Microscopy, Fluorescence / Microtubules / Microvilli / Parathyroid Hormone / Parathyroidectomy / Peptide Fragments / Phosphates / RNA / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Thyroidectomy (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00100.2006 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16985216 ● Search Scopus @ Elsevier (PMID): 16985216 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00100.2006 (DOI: 10.1152/ajprenal.00100.2006, PubMed: 16985216)
78.	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. (要約) 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). (キーワード) Adult / Blood Glucose / Cross-Over Studies / Energy Metabolism / Fatty Acids, Nonesterified / Humans / Insulin / Isomaltose / Male / Oxidation-Reduction / Postprandial Period (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.metabol.2006.09.005 (文献検索サイトへのリンク) ● 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)
79.	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. (要約) 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. (キーワード) 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 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18356582 ● Search Scopus @ Elsevier (PMID): 18356582 (PubMed: 18356582)
80.	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. (要約) 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. (キーワード) Administration, Oral / Adult / カルシウム (calcium) / Cross-Over Studies / Fibroblast Growth Factors / ホメオスタシス (homeostasis) / Humans / Male / Parathyroid Hormone / Phosphates / Vitamin D (出版サイトへのリンク) ● Publication site (DOI): 10.1038/sj.ki.5002000 (文献検索サイトへのリンク) ● 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)
81.	宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 : リンとビタミンDの相互作用, 整形・災害外科, Vol.49, No.12, 1365-1370, 2006年. (キーワード) Transporter / Kidney / FGF23 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520291855700655232 (CiNii: 1520291855700655232)
82.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.tox.2006.08.009 (文献検索サイトへのリンク) ● 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)
83.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/sj.ejcn.1602420 (文献検索サイトへのリンク) ● 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)
84.	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. (要約) 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. (キーワード) Animals / Calcium / Calcium, Dietary / Dihydroxycholecalciferols / Duodenum / Humans / Immobilization / Intestinal Absorption / Rats / Rats, Wistar (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00774-006-0686-z (文献検索サイトへのリンク) ● 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)
85.	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. (キーワード) Animals / Calcium Signaling / Cell Line / Endothelial Cells / Kidney Tubules, Proximal / Phosphates / 活性酸素 (reactive oxygen species) / シグナル伝達 (signal transduction) / Swine (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.advenzreg.2006.01.003 (文献検索サイトへのリンク) ● 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)
86.	宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 : 栄養素の代謝と生理機能, 病態栄養専門師のための病態栄養ガイドブック, 14-19, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488265 (CiNii: 1020000781987488265)
87.	宮本賢一, 竹谷豊, 伊藤美紀子, 瀬川博子 : ナトリウム依存症リントランスポータ-の調節機構, Annual Review 腎臓, 216-220, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488258 (CiNii: 1020000781987488258)
88.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbaexp.2005.11.003 (文献検索サイトへのリンク) ● 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)
89.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/j.1523-1755.2005.00505.x (文献検索サイトへのリンク) ● 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)
90.	Naomi Tanoue, Akira Takahashi, Keinosuke Okamoto, Yoshio Fujii, Yutaka Taketani, Nagakatsu Harada, Masayuki Nakano and Yutaka Nakaya : A pore-forming toxin produced by Aeromonas sobria activates cAMP-dependent Cl- secretory pathways to cause diarrhea, FEMS Microbiology Letters, Vol.242, No.2, 195-201, 2005. (要約) Aeromonas sobria hemolysin (ASH) is one of the major virulence factors produced by A. sobria, a human pathogen that causes diarrhea. We investigated the effects of ASH on Cl(-) transport in human colonic epithelial cells. ASH increased short-circuit currents (Isc) and (125)I efflux from Caco-2 cells, indicating ASH activate Cl(-) secretion. Additions of inhibitors of cyclic AMP dependent Cl(-) channels, glybenclamide and NPPB suppressed the Isc and (125)I efflux increases induced by ASH. And ASH increased the intracellular cyclic AMP concentration. Moreover, ASH stimulated fluid accumulation in the iliac loop test, and glybenclamide and NPPB suppressed this fluid accumulation. Thus, cAMP-dependent Cl(-) secretory pathway could be related with diarrhea induced by A. sobria. (キーワード) Aeromonas / Animals / 細菌毒素 (bacterial toxins) / Caco-2 Cells / Cells, Cultured / Chloride Channels / Chlorides / Cyclic AMP / Diarrhea / Hemolysin Proteins / Humans / Intestinal Mucosa / Mice (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.femsle.2004.11.009 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15621437 ● Search Scopus @ Elsevier (PMID): 15621437 ● Search Scopus @ Elsevier (DOI): 10.1016/j.femsle.2004.11.009 (DOI: 10.1016/j.femsle.2004.11.009, PubMed: 15621437)
91.	竹内里美, 竹内晴美, 奥村仙示, 新井英一, 竹谷豊, 山田静恵, 高橋保子, 武田英二 : 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年.
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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.metabol.2004.03.004 (文献検索サイトへのリンク) ● 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.	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. (要約) 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. (キーワード) Animals / Diet / Homeostasis / Humans / Hypophosphatemia, Familial / Osteomalacia / Phosphates (出版サイトへのリンク) ● Publication site (DOI): 10.1111/j.1582-4934.2004.tb00274.x (文献検索サイトへのリンク) ● 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)
94.	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. (要約) 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. (キーワード) Animals / Boron Compounds / Calcium / Cell Line / Cytoplasm / Inositol 1,4,5-Trisphosphate / Kidney Tubules, Proximal / Kinetics / Microscopy, Confocal / Phosphates / Rats (出版サイトへのリンク) ● Publication site (DOI): 10.1016/S0006-291X(03)00750-2 (文献検索サイトへのリンク) ● 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)
95.	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. (要約) 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. (キーワード) Bone and Bones / Calcium, Dietary / Food Analysis / Food Supply / Humans / 日本 (Japan) / Nutritional Requirements / リン (phosphorus) / Phosphorus, Dietary (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12171429 ● Search Scopus @ Elsevier (PMID): 12171429 (PubMed: 12171429)
96.	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. (要約) 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. (キーワード) CENTRAL-NERVOUS-SYSTEM / SMOOTH-MUSCLE CELLS / PROTEIN-KINASE-1 BMK1 / TRANSDUCTION PATHWAY / NEURONAL DIFFERENTIATION / CEREBRAL-ISCHEMIA / TYROSINE KINASES / OXYGEN RADICALS / GENE-EXPRESSION / JUN PROMOTER (出版サイトへのリンク) ● Publication site (DOI): 10.1074/jbc.M111790200 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11782488 ● CiNii @ 国立情報学研究所 (CRID): 1573950401500650880 ● Search Scopus @ Elsevier (PMID): 11782488 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111790200 (DOI: 10.1074/jbc.M111790200, PubMed: 11782488, CiNii: 1573950401500650880)
97.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/S0005-2736(01)00384-4 (文献検索サイトへのリンク) ● 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)
98.	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. (キーワード) elongation / promoter / run-on assay
99.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s007740170012 (文献検索サイトへのリンク) ● 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)
100.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1046/j.1471-4159.2001.00488.x (文献検索サイトへのリンク) ● 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)
101.	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. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s101570170002 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-17944363928 (DOI: 10.1007/s101570170002, Elsevier: Scopus)
102.	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.
103.	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.
104.	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. (要約) 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. (キーワード) Aged / Basal Metabolism / Calorimetry, Indirect / Dietary Carbohydrates / Dietary Fats / Dietary Proteins / エネルギー代謝 (energy metabolism) / Fasting / Fatty Acids, Nonesterified / Food / Glycogen / Humans / Liver Cirrhosis / Middle Aged / Oxidation-Reduction (出版サイトへのリンク) ● Publication site (DOI): 10.1016/S0899-9007(99)00149-5 (文献検索サイトへのリンク) ● 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)
105.	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.
106.	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.
107.	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. (キーワード) Vitamin D3 / monocyte
108.	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. (キーワード) vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release
109.	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. (キーワード) vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release

学術論文(紀要・その他):

1.	増田真志, 塩﨑雄治, 竹谷豊, 宮崎淳 : 最前線慢性腎臓病の合併症とlipotoxicity, ファルマシア, Vol.58, No.4, 329-333, 2022年. (徳島大学機関リポジトリ) ● Metadata: 118681 (出版サイトへのリンク) ● Publication site (DOI): 10.14894/faruawpsj.58.4_329 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.14894/faruawpsj.58.4_329 (徳島大学機関リポジトリ: 118681, DOI: 10.14894/faruawpsj.58.4_329)
2.	宮本賢一, 竹谷豊 : 食餌性リンによる血管障害, 日本透析医会雑誌, Vol.30, No.1, 128-133, 2015年.
3.	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.
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. (要約) 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. (キーワード) Diet Therapy / Dietary Proteins / Disease Progression / Food, Formulated / Humans / Kidney Failure, Chronic / Phosphates / Phosphorus, Dietary / Renal Osteodystrophy (出版サイトへのリンク) ● Publication site (DOI): 10.1159/000101004 (文献検索サイトへのリンク) ● 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. (要約) 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. (キーワード) Animals / Diabetes Mellitus, Type 2 / Disease Models, Animal / Gene Expression Regulation / Glycemic Index / Humans / Oxidative Stress / PPAR alpha / PPAR gamma / Postprandial Period (出版サイトへのリンク) ● Publication site (DOI): 10.1159/000107089 (文献検索サイトへのリンク) ● 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.	竹内晴美, 奥村仙示, 中村多希, 竹内里美, 新井英一, 竹谷豊, 藤井正彦, 三宅秀則, 田代正記, 武田英二 : 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年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1570291226541281920 (CiNii: 1570291226541281920)

学術レター:

1.	Masashi Suzue, Ken-ichi Suga, Yutaka Taketani, Ryuji Nakagawa and Maki Urushihara : Chylous ascites complicating perinatal severe hypophosphatasia in an infant on high-setting ventilation and enzyme replacement therapy., Pediatrics International, Vol.65, No.1, 2023. (キーワード) Infant / Humans / Hypophosphatasia / Enzyme Replacement Therapy / Chylous Ascites / Respiration / Immunoglobulin G / Alkaline Phosphatase (出版サイトへのリンク) ● Publication site (DOI): 10.1111/ped.15585 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37475513 ● Search Scopus @ Elsevier (PMID): 37475513 ● Search Scopus @ Elsevier (DOI): 10.1111/ped.15585 (DOI: 10.1111/ped.15585, PubMed: 37475513)

総説・解説:

1.	増田真志, 山本菜摘, 竹谷豊 : 腎臓病に対するビタミンAの影響, ビタミン, Vol.97, No.7, 340-343, 2023年7月. (徳島大学機関リポジトリ) ● Metadata: 119612 (徳島大学機関リポジトリ: 119612)
2.	竹谷豊 : 慢性腎臓病CKDとたんぱく質栄養, 食肉の多様性と未来国産食肉の安全・安心2021, 56-64, 2022年3月.
3.	竹谷豊 : ビタミンDと加齢, アグリバイオ, Vol.5, No.11, 8-12, 2021年10月. (キーワード) カルシウム / ホルモン / 栄養 / 日興曝露 / エイヨウ / ニッコウバクロ (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523106606074847744 (CiNii: 1523106606074847744)
4.	竹谷豊, 亀井優輝 : ビタミン・微量元素不足が生じやすい状況と補充で期待される効果, Medical Practice, Vol.38, No.9, 1343-1348, 2021年9月.
5.	竹谷豊 : リンと心血管疾患, 薬事日報, No.12010, 14-15, 2018年4月.
6.	竹谷豊, 伊美友紀子, 多々納浩, 福田詩織, 増田真志 : 児童生徒の食と健康(2)児童生徒の成長と骨の健康維持, 栄養教諭 : 食育読本, No.46, 18-22, 2017年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523388080466160256 (CiNii: 1523388080466160256)
7.	竹谷豊, 伊美友紀子, 楢﨑遥子, 増田真志, 奥村仙示 : 教授就任記念講演慢性腎臓病におけるリン代謝異常と食事管理, 四国医学雑誌, Vol.72, No.5, 171-176, 2016年12月. (要約) Chronic kidney disease is a common disease impacting more than 13 million individuals in Japan. CKD causes various complications including cardiovascular disease, infectious disease, and metabolic bone disease. Systemic mineral disorder caused by CKD increases cardiovascular disease and mortality risks as well as metabolic bone disease. Now, it is known as CKD-mineral and bone disease(CKD-MBD)characterized by blood biochemical abnormalities, bone abnormalities and extraskeletal calcification. Management of CKD-MBD is important to decrease cardiovascular disease and mortality risks. Hyperphosphatemia is a primary cause of CKD-MBD. Not only correction of hyperphosphatemia but also decrease in dietary phosphorus load is a key strategy for management of CKD-MBD. Here we will provide an overview of disorder of phosphorus metabolism and dietary management in CKD patients. (徳島大学機関リポジトリ) ● Metadata: 110399 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050282812441828608 (徳島大学機関リポジトリ: 110399, CiNii: 1050282812441828608)
8.	Yutaka Taketani, Fumihiko Koiwa and Keitaro Yokoyama : Management of phosphorus load in CKD patients., Clinical and Experimental Nephrology, Vol.21, No.Suppl 1, 27-36, Nov. 2016. (要約) Disturbances in mineral and bone metabolism play a critical role in the pathogenesis of cardiovascular complications in patients with chronic kidney disease (CKD). The term "renal osteodystrophy" has recently been replaced with "CKD-mineral and bone disorder (CKD-MBD)", which includes vascular calcification as well as bone abnormalities. In Japan, proportions of the aged and long-term dialysis patients are increasing which makes management of vascular calcification and parathyroid function increasingly more important. There are three main strategies to manage phosphate load: phosphorus dietary restriction, administration of phosphate binder and to ensure in the CKD 5D setting, an adequate dialysis. (キーワード) Animals / Bone Diseases, Metabolic / Chronic Kidney Disease-Mineral and Bone Disorder / Humans / Hyperphosphatemia / Minerals / Phosphorus / Phosphorus, Dietary / Renal Insufficiency, Chronic (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10157-016-1360-y (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27896453 ● Search Scopus @ Elsevier (PMID): 27896453 ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-016-1360-y (DOI: 10.1007/s10157-016-1360-y, PubMed: 27896453)
9.	竹井悠一郎, 谷村綾子, 竹谷豊 : 微量元素・ビタミン不足の評価 (特集栄養障害患者の評価), 内分泌·糖尿病·代謝内科, Vol.43, No.3, 190-195, 2016年9月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523951029857076608 (CiNii: 1523951029857076608)
10.	竹谷豊, 伊美友紀子, 杉原康平 : ビタミン・ミネラルと糖尿病, ホルモンと臨床, Vol.62, No.3, 211-215, 2016年3月.
11.	奥村仙示, 多々納浩, 梶浦大資, 山口智勢, 増田真志, 竹谷豊 : 生活習慣病の要:栄養教育と実践, Clinical Calcium, Vol.26, No.3, 101-106, 2016年.
12.	竹谷豊 : 生活習慣病予防のための生活習慣, めんたるへるす, No.64, 40-44, 2015年12月.
13.	武田英二, 山本浩範, 竹谷豊 : 新規シグナルとしてのリン酸(<特集>ビタミンB研究委員会平成26年度シンポジウム「ビタミン・バイオファクターの生理機能に関する最新の話題」), ビタミン, Vol.89, No.8, 393-396, 2015年8月. (要約) 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. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205701585536 (CiNii: 1390001205701585536)
14.	武田英二, 山本浩範, 竹谷豊 : 新規シグナルとしてのリン酸, ビタミン, Vol.89, No.8, 393-396, 2015年8月.
15.	竹谷豊, 伊美友紀子, Abuduli Maerjianghan : リンの有する新しい作用, Clinical Calcium, Vol.25, No.7, 1015-1021, 2015年6月. (要約) Phosphorus is an essential nutrient for bone formation by forming hydroxyapatite with calcium. Simultaneously, phosphorus is also a component of high energy bond of ATP, nucleic acids, and phospholipids. Recent studies have demonstrated that excess or lack of dietary phosphorus intake may cause vascular dysfunction, cardiac hypertrophy, and impaired glucose tolerance. Here, we introduce recent findings about the effects of high or low dietary phosphorus intake on several organs except for bone. (キーワード) Adenosine Triphosphate / Animals / Calcium / Cardiomegaly / Durapatite / Endothelium, Vascular / Glucose Intolerance / Humans / Hypertension / Insulin Resistance / Mice / Nucleic Acids / Osteogenesis / Phospholipids / Phosphorus / Phosphorus, Dietary / Vascular Calcification (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26119314 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942605529 (PubMed: 26119314, Elsevier: Scopus)
16.	宮本賢一, 竹谷豊 : 食餌性リンによる血管障害, 日本透析医学会雑誌, Vol.30, No.1, 128-133, 2015年4月.
17.	武田英二, 奥村仙示, 竹谷豊, 山本浩範 : 小児疾患および成人疾患からみたビタミンD栄養学, ビタミン, Vol.88, No.10, 499-506, 2014年10月. (要約) 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. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680676820096 (CiNii: 1390282680676820096)
18.	武田英二, 奥村仙示, 竹谷豊, 山本浩範 : 小児疾患および成人からみたビタミンD栄養学, ビタミン, Vol.10, 499-506, 2014年.
19.	奥村仙示, 大南博和, 竹谷豊, 武田英二 : 「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年.
20.	奥村仙示, 足立知咲, 周蓓, 竹谷豊, 武田英二 : 「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年.
21.	奥村仙示, 竹谷豊, 武田英二 : 「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年.
22.	竹谷豊, 大南博和, 中橋乙起, 池田翔子 : ビタミンD結合タンパク質の遺伝子多型と疾患(<特集>「ビタミンと遺伝子多型」-ビタミンD-), ビタミン, Vol.87, No.9, 506-513, 2013年9月. (要約) Vitamin D binding protein (DBP), which is also known as a group-specific component (GC)-globulin, is a major plasma carrier protein for vitamin D and its metabolites. DBP is also known as an actin scavenger and a precursor of GC protein-derived macrophage activating factor (GC-MAF). This multifunction protein plays a role in the determination of serum 25-hydroxyvitamin D levels and regulation of the immune system. Therefore, genetic variants of DBP may affect risks of various diseases related with vitamin D levels and the immune system. Until now, various protein and genetic polymorphisms of DBP have been identified. Especially, Gc1S, Gc1F and Gc2 are well-known polymorphisms characterized by isoelectrophoresis, which are derived from two missense variants of DBP gene encoding D432E (rs7041) and T436K (rs4588). In this review, we discuss some relationships between DBP genotypes and common disease risk including osteoporosis, cancer and diabetes. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680677288320 (CiNii: 1390282680677288320)
23.	中尾真理, 山本浩範, 中橋乙起, 阿部航太郎, 竹谷豊, 武田英二 : 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, 四国医学雑誌, Vol.68, No.5-6, 270-271, 2012年12月.
24.	武田英二, 山本浩範, 奥村仙示, 竹谷豊 : 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, 2012年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523106605284363136 (CiNii: 1523106605284363136)
25.	武田英二, 奥村仙示, 山本浩範, 竹谷豊 : うつ病と栄養 (特集メンタルヘルスと栄養), 四国医学雑誌, Vol.68, No.1, 3-8, 2012年4月. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 97911 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050564287417308416 (徳島大学機関リポジトリ: 97911, CiNii: 1050564287417308416)
26.	武田英二, 山本浩範, 奥村仙示, 竹谷豊 : 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, 2012年2月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1572824500597643264 (CiNii: 1572824500597643264)
27.	竹谷豊, 福澤健治 : ビタミンと生活習慣病(特集:生活習慣病の栄養管理), 成人病と生活習慣病, Vol.41, No.11, 1343-1350, 2011年11月.
28.	竹谷豊, 山本浩範, 武田英二, 宮本賢一 : ビタミンDとリン代謝, --- 加齢遺伝子とのかかわり ---, CLINICAL CALCIUM, Vol.16, No.7, 1137-1142, 2006年7月.
29.	竹谷豊, 山本浩範, 武田英二 : 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, 2005年5月.
30.	武田英二, 奥村仙示, 竹谷豊 : 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, 2004年7月.
31.	武田英二, 竹谷豊 : 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, 2004年6月.
32.	武田英二, 竹谷豊 : 生体におけるリンの役割と制御, 腎不全とリン, 17-21, 2004年6月.
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. (要約) 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. (キーワード) 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 (文献検索サイトへのリンク) ● 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.	武田英二, 新井英一, 竹谷豊 : 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, 2003年10月.
35.	武田英二, 竹谷豊, 三宅秀則 : 肝疾患における低栄養の病態と治療, 肝·胆·膵, Vol.47, No.1, 93-98, 2003年7月.
36.	竹谷豊, 武田英二 : 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, 2003年2月.
37.	武田英二, 梨木邦剛, 竹谷豊 : ミネラルの生体での代謝と吸収, FOOD Style 21, Vol.7, No.2, 41-46, 2003年2月.
38.	奥村仙示, 中村多希, 津田紀子, 竹谷豊, 國清紀子, 高橋保子, 武田英二 : 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年.
39.	竹谷豊, 梨木邦剛, 一色政志, 武田英二 : 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年. (キーワード) 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
40.	竹谷豊, 大久保公美, 小林くみ, 武田英二 : 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年.
41.	Eiji Takeda, Kyoko Morita, Yutaka Taketani, Hironori Yamamoto and Ken-ichi Miyamoto : Renal handling of phosphate, Calcium In Internal Medicine, 137-148, 2002.

国際会議:

1.	Mori Yuki, Masashi Masuda, Nguyen The Anh, Kohta Ohnishi, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse adipocytes, The 3rd Japan-France Space Nutrition & Medicine Symposium, Kyoto, Nov. 2023.
2.	Masashi Masuda, Adachi Yuichiro and Yutaka Taketani : All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal, The 3rd Japan-France Space Nutrition & Medicine Symposium, Kyoto, Nov. 2023.
3.	Mori Yuki, Masashi Masuda, Yoshida-Shimizu Risa, Nguyen The Anh, Kohta Ohnishi, Hirokazu Ohminami, Hamada Koichiro and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse adipocytes, Kern Lipid Conference 2023, Colorado, Aug. 2023.
4.	Yutaka Taketani : Future direction for dietary therapy of chronic kidney disease, The International Workshop on Gut-kidney Axis and Chronic Kidney Disease, Tokyo, Mar. 2023.
5.	Yutaka Taketani : Dietary therapy for hyperphosphatemia in CKD, The International Workshop on Gut-kidney Axis and Chronic Kidney Disease, Tokyo, Mar. 2023.
6.	Yamao Shoko, Kanno Takeo, Shimazui Miyuki, Yoshimura Ashio, Koiwa Fumihiko and Yutaka Taketani : Re-evaluation of potassium and phosphorus restriction in CKD - A study using a daily menu, The International Workshop on Gut-kidney Axis and Chronic Kidney Disease, Tokyo, Mar. 2023.
7.	Hamamoto Riko, Hirokazu Ohminami, Shu Wakino and Yutaka Taketani : Effectiveness of protein restriction diet on chronic kidney disease: a systematic review, The International Workshop on Gut-kidney Axis and Chronic Kidney Disease, Tokyo, Mar. 2023.
8.	Okumura Yosuke, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Effect of phosphate on intestinal zinc absorption in 5/6 nephrectomized rats, 第22回国際栄養学会議, Online, Dec. 2022.
9.	Tsumura Ayari, Hisami Okumura, Kawakami Hana, Yamamoto Shiori, Ohura Mayu, Tatano Hiroshi, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Investigation of Amino Acids and Fatty Acids Profiles of Japanese Diets Using the Food Exchange Chart for Diabetes Diet, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
10.	Mori Yuki, Masashi Masuda, Yoshida-Shimizu Risa, Aoyagi Saki, Adachi Yuichiro, Kohta Ohnishi, Hirokazu Ohminami, Hamada Koichiro and Yutaka Taketani : All-trans retinoic acid induces lipolysis via activation of autophagy in mouse adipocytes, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
11.	Takikawa Masaki, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Dietary combination of sucrose and linoleic acid synergistically accumulates the intramuscular lipid and decreases the muscle strength in Zucker diabetic fatty rats, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
12.	Yuki Kamei, Okumura Yosuke, Adachi Yuichiro, mori Yuki, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Inhibitory Mechanism of Ectopic Calcification during Growth Period, The American Society for Bone and Mineral Research 2022 Annual Meeting, Online, Sep. 2022.
13.	Yuichiro Adachi, Masashi Masuda, Kohei Sasaki, Hirokazu Ohminami, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Hypervitaminosis A Contributes to Kidney Injury Through Excessive Endoplasmic Reticulum Stress in CKD, ASN Kidney Week 2021, Nov. 2021.
14.	Kohta Ohnishi, Moe FUJIMOTO, Maiko SAKAI, Teppei FUKUDA, Aika OHNISHI, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : Exploration of bioactive food factors for the control of autophagy flux, The 7th International Conference on Food Factors, Dec. 2019. (キーワード) オートファジー (autophagy) / 質量分析法 (mass spectrometry)
15.	Maiko SAKAI, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Taichi HARA and Yutaka Taketani : Elucidation of the molecular mechanism underlying lysosomal activation in J774.1 cells by isorhamnetin treatment, The 7th International Conference on Food Factors, Dec. 2019.
16.	Oda Naoko, Sugihara Kohei, Miho Ikeda, Yuho Higashimura, Takashi Uebanso, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., American Society of Nephrolody Kidney Week 2019, Washington, D.C., Nov. 2019.
17.	Fukuda-Tatano Shiori, Hironori Yamamoto, Nakahashi Otoki, Yoshikawa Ryouhei, Hayashi Mayu, Kishimoto Maki, Yukiko Imi, Yamanaka-Okumura Hisami, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Regulation of α-klotho Expression by Dietary Phosphate During Growth Periods, ASBMR 2019 Annual Meeting, Sep. 2019.
18.	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.
19.	Maiko SAKAI, Kohta Ohnishi, Teppei FUKUDA, Masashi Masuda, Naomi Kanoh, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : mTORC2 signaling is critical for lysosomal activation by isorhamnetin treatment in J774.1., FAOPS2019, Mar. 2019. (キーワード) lysosome / mTORC2 / isorhamnetin
20.	Serina Kabutoya, Masashi Masuda, Yuichiro Adachi, Yilimulati Timamu, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Hypervitaminosis A contributes to abnormal iron metabolism in CKD, American Society of Nephrology Kidney Week 2018 (San Diego, CA), Oct. 2018.
21.	Mayu Hayashi, Shiori Fukuda, Maki Kishimoto, Hironori Yamamoto, Masashi Masuda and Yutaka Taketani : High phosphate diet before pregnancy dysregulates phosphate metabolism in neonatal offspring mice, American Society of Nephrology Kidney Week 2018 (San Diego, CA), Oct. 2018.
22.	Yoshida Risa, Masashi Masuda, Mori Yuki, Niida Yuki, Adachi Yuichiro, Kohta Ohnishi, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : Sulforaphane induces lipolysis via lipophagy in mouse adipocyte, Kern Lipid Conference, Vail, Colorado, Aug. 2018.
23.	Niida Yuki, Masashi Masuda, Yoshizawa Aika, Adachi Yuichiro, Yimamu Yilimulati, Kabutoya Serina, Yoshida Risa, Hisami Okumura, Yoshichika Kawai, Miyazaki Makoto, Hironori Yamamoto and Yutaka Taketani : Abnormal lipid metabolism in skeletal muscle mediates chronic kidney disease-induced sarcopenia, ASN Kidney Week 2017, New Orleans, Nov. 2017.
24.	Hi Tatano, Hisami Okumura, D Kajiura, Masashi Masuda, A Hirayama, T Soga, M Tomita and Yutaka Taketani : Meat and fish consumption lead to differences in plasma N-acetylaspartate and trimethylamine N-oxide concentrations in healthy men, 12th Metabolomics Society Conference, Brisbane, Australia, Jun. 2017.
25.	Yoko Narasaki, Michiyo Yamasaki, Misaki Katsumoto and Yutaka Taketani : Development of Phosphatemic Index for Evaluation of Phosphate-Containing Foods in Healthy Japanese., Kidney Week 2016, Chicago, Nov. 2016.
26.	Yukiko Imi, Masashi Masuda, Maerjianghan Abuduli, Norie Yabiki, Hisami Okumura, Makoto Miyazaki and Yutaka Taketani : High phosphorus induces the lipolysis through endoplasmic reticulum stress, Kern Lipid Conference, Vail, Colorado, USA, Aug. 2016.
27.	Hiroshi Tatano, Hisami Okumura, Daisuke Kajiura, C Kondo, A Hirayama, Kazuaki Mawatari, Yoshichika Kawai, Masashi Masuda and Yutaka Taketani : Exploring the impact of consuming different types of meat on metabolome profiles using a GC-MS metabolomics approach, 11th Metabolomics Society Conference, Dublin, Jul. 2016.
28.	Yoko Narasaki, Sayaka Matsuura, Mayumi Morinishi, Michiyo Yamasaki, Misaki Katsumoto, Tsuneyuki Noda and Yutaka Taketani : Development of Phosphatemic Index for Evaluation of Phosphate-containing Foods, XVIII International Congress on Nutrition and Metabolism in Renal Disease (ICRNM2016), Okinawa Convention Center, Ginowan, Okinawa, Apr. 2016.
29.	Ken-ichi Miyamoto and Yutaka Taketani : Phosphorus content in daily foods and drinks: Does it matter?, XVIII International Congress on Nutrition and Metabolism in Renal Desease(ICRNM2016)., Apr. 2016.
30.	福田詩織, Hironori Yamamoto, Masashi Masuda, 中尾真理 and Yutaka Taketani : Regulation of a-klotho expression by dietary phosphate during growth periods., ASN 2015 Renal week, San Diego, Nov. 2015.
31.	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.
32.	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.
33.	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.
34.	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.
35.	Yutaka Taketani, Haruka Ueda, Abuduli Maerjianghan and Hironori Yamamoto : Correction of Hyperphosphosphatemia by Dietary Phosphorus Restriction or Phosphorus Binder Similarly Ameliorates Vascular Complications and Mineral Disorders in CKD Rats, American Heart Association Scientific Sessions 2014 Nov. 15-19, 2014 - McCormick Place, Chicago Il., Nov. 2014.
36.	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.
37.	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.
38.	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.
39.	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.
40.	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.
41.	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.
42.	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.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
48.	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.
49.	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.
50.	森本優香, 佐久間理英, 太田紘之, 梅田見名子, 石川真, 竹谷豊, 武田英二, 新井英一 : 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, 2013年1月.
51.	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.
52.	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.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	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.
59.	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.
60.	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.
61.	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.
62.	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.
63.	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.
64.	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.
65.	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.
66.	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.
67.	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.
68.	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.
69.	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.
70.	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.
71.	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.
72.	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.
73.	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.
74.	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.
75.	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.
76.	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.
77.	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.
78.	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.
79.	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.
80.	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.
81.	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.
82.	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.
83.	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.
84.	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.
85.	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.
86.	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.
87.	竹谷豊, K. Nashiki, N. Sawada, 山本浩範, M. Ichikawa, 森田恭子, 新井英一, 武田英二 : 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, 2003年9月.
88.	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.
89.	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.
90.	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.
91.	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.
92.	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.
93.	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.

国内講演発表:

1.	池田翔子, 山本浩範, 増田真志, 中橋乙起, 橋本脩平, 向原理恵, 中尾真理, 竹谷豊, 武田英二 : 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, 竹谷豊, 山本浩範, 阿望幾久子, 田中更沙, 新井英一, 大南博和, 奥村仙示, 武田英二 : 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, 阿望幾久子, 竹谷豊, 上番増喬, 佐藤佳瑞智, 深谷牧子, 新井英一, 小金井恵, 佐々木一, 山本浩範, 武田英二 : 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.	伊勢孝之, 石井亜由美, 西川幸治, 門田宗之, 上野理絵, 八木秀介, 大南博和, 竹谷豊, 佐田政隆 : 進歩するSHDに対する治療と心臓リハビリテーション, 第30回日本心臓リハビリテーション学会学術集会, 2024年7月.
5.	林下菜奈, 竹原和可子, 滝川真輝, 大南博和, 増田真志, 竹谷豊 : 妊娠中の食餌性リン負荷が仔に及ぼす影響について, 第8回日本CKD-MBD学会学術集会・総会, 2024年3月.
6.	大南博和, 北村彩乃, 増田真志, 伊勢孝之, 八木秀介, 佐田政隆, 竹谷豊 : 心不全マウスに対する高脂肪食と運動の併用効果，優秀演題アワードセッショ, 日本心臓リハビリテーション学会第7回四国支部地方会, 2024年3月.
7.	Nguyen The Anh, Masashi Masuda, Mori Yuki, Adachi Yuichiro, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse hepatocytes, 第46回日本分子生物学会年会, Dec. 2023.
8.	丸山祐昌, 増田真志, 木村玲奈, 山本菜摘, 大南博和, 竹谷豊 : 小脳顆粒細胞のATP量に対する細胞外リン濃度の影響, 第56回日本栄養・食糧学会中国・四国支部大会, 2023年10月.
9.	竹谷豊, 足立雄一郎, 山本菜摘, 大南博和, 増田真志 : 慢性腎臓病とビタミンA, フォーラム2023:衛生薬学・環境トキシコロジー, 2023年9月.
10.	石井亜由美, 西川幸治, 門田宗之, 楠瀬賢也, 八木秀介, 大南博和, 内藤紘一, 竹谷豊, 佐田政隆 : 情報発信WEB 「リカバルクラブ」を用いた多職種患者教育の取り組み, 第71回日本心臓病学会学術集会，2023年9月8日(金)∼10日(日)，東京, 2023年9月.
11.	山本浩範, 中橋乙起, 石黒真理子, 増田真志, 武田英二, 岩野正之, 岸愼治, 竹谷豊 : 炎症時におけるリン・ビタミンDの役割と腎臓での代謝調節機構の解明, 第70回日本栄養改善学会学術総会, 2023年9月.
12.	伊勢孝之, 石井亜由美, 西川幸治, 上野理恵, 門田宗之, 八木秀介, 大南博和, 内藤紘一, 竹谷豊, 佐田政隆 : 遠隔伴走型心リハ「リカバル」による新たな在宅心リハの取り組み, 第29回日本心臓リハヒリテーション学会学術集会, 2023年7月.
13.	大南博和, 北村彩乃, 松原未奈, 増田真志, 伊勢孝之, 八木秀介, 佐田政隆, 竹谷豊 : 動物モデルから探る心リハ栄養としての糖・脂質組成の意義, 第29回日本心臓リハビリテーション学会学術集会, 2023年7月.
14.	森優樹, 増田真志, Anh The Nguyen, 大西康太, 大南博和, 濱田広一郎, 竹谷豊 : レチノイン酸によるリポファジーへの影響, 日本ビタミン学会第75回大会, 2023年6月.
15.	山本菜摘, 増田真志, 足立雄一郎, 春本恵里花, 野邊悠太郎, 大南博和, 山本浩範, 竹谷豊 : 慢性腎臓病モデルマウスの腎臓内ビタミンA代謝調節機構, 日本ビタミン学会第75回大会, 2023年6月.
16.	伊勢孝之, 石井亜由美, 西川幸治, 門田宗之, 八木秀介, 大南博和, 竹谷豊, 佐田政隆 : 遠隔伴走型心臓リハヒリテーション「リカバル」を用いた新たな取り組み, 日本心臓リハヒリテーション学会第6回四国支部地方会, 2023年3月.
17.	大南博和, 北村彩乃, 松原未奈, 増田真志, 伊勢孝之, 八木秀介, 佐田政隆, 竹谷豊 : 動物モデルから探る病期別心リハ栄養の可能性, 第12回日本リハビリテーション栄養学会学術集会, 2023年1月.
18.	北村彩乃, 大南博和, 松原未奈, 増田真志, 伊勢孝之, 八木秀介, 佐田政隆, 竹谷豊 : 高脂肪食が心不全マウスの骨格筋エネルギー代謝に及ぼす影響, 第26回日本病態栄養学会年次学術集会, 2023年1月.
19.	山本菜摘, 増田真志, 春本恵里花, 野邊悠太郎, 大南博和, 竹谷豊 : 慢性腎臓病モデルマウスの腎臓内ビタミンA代謝変化, 第26回日本病態栄養学会年次学術集会, 2023年1月.
20.	野邊悠太郎, 増田真志, 佐々木晧平, 足立雄一郎, 大南博和, 竹谷豊 : 慢性腎臓病の腎臓における all-trans retinoic acid 水酸化酵素 Cyp26b1 制御機構の解明, 第55回日本栄養・食糧学会中国・四国支部大会, 2022年10月.
21.	竹谷豊 : 栄養素としてのリンの役割と課題, 第31回無機リン化学討論会, 2022年9月.
22.	亀井優輝, 大南博和, 増田真志, 竹谷豊 : 成長期には血中リン濃度が高くても血管石灰化が生じないのはなぜか?, 第69回日本栄養改善学会学術総会, 2022年9月.
23.	滝川真輝, 大南博和, 増田真志, 竹谷豊 : スクロースとリノール酸は相乗的に筋内脂肪蓄積と筋力低下を引き起こす, 第69回日本栄養改善学会学術総会, 2022年9月.
24.	奥村陽介, 酒井晶子, 阿部船太郎, 大南博和, 増田真志, 竹谷豊 : 慢性腎臓病に伴う低亜鉛血症の発症機序解明, 第10回日本腎栄養代謝研究会学術集会・総会, 2022年7月.
25.	春本恵里花, 増田真志, 佐々木晧平, 足立雄一郎, 森優樹, 大南博和, 山本浩範, 竹谷豊 : 高齢マウスの腎臓におけるビタミンA代謝関連遺伝子発現変化, 日本ビタミン学会第74回大会, 2022年6月.
26.	増田真志, 足立雄一郎, 竹谷豊 : 骨格筋の筋繊維タイプ変化に対するビタミンAの影響, 第372回脂溶性ビタミン総合研究委員会プログラム, 2022年6月.
27.	北村彩乃, 大南博和, 増田真志, 奥村仙示, 伊勢孝之, 八木秀介, 福田大受, 山田博胤, 佐田政隆, 竹谷豊 : 運動介入中の脂質摂取の違いが心不全マウスの病態に及ぼす影響, 第28回日本心臓リハビリテーション学会学術集会, 2022年6月.
28.	滝川真輝, 大南博和, 増田真志, 竹谷豊 : スクロースとリノール酸の豊富な食餌は筋繊維内脂肪を増加させる, 第63回日本生化学会中国・四国支部例会, 2022年5月.
29.	森優樹, 増田真志, 吉田里沙, 青柳咲紀, 大西康太, 大南博和, 濱田広一郎, 竹谷豊 : レチノイン酸によるオートファジーを介した脂肪分解への影響, 第63回日本生化学会中国・四国支部例会, 2022年5月.
30.	佐々木晧平, 増田真志, 足立雄一郎, 春本恵里花, 大南博和, 奥村仙示, 山本浩範, 竹谷豊 : 慢性腎臓病における腎臓の小胞体ストレスを介した all-trans retinoic acid 水酸化酵素Cyp26b1制御機構の解明, 第 6 回日本CKD-MBD研究会学術集会・総会, 2022年3月.
31.	竹谷豊 : CKDの栄養管理におけるビタミン，第24回，第25回日本病態栄養学会年次学術集会合同パネルディスカッション, 2022年1月.
32.	北村彩乃, 大南博和, 増田真志, 奥村仙示, 伊勢孝之, 八木秀介, 福田大受, 山田博胤, 佐田政隆, 竹谷豊 : 運動および栄養介入が心不全マウスの病態に及ぼす影響, 日本心臓リハビリテーション学会第 5 回四国支部地方会, 2022年1月.
33.	木村玲奈, 増田真志, 山本菜摘, 野邊悠太郎, 大南博和, 奥村仙示, 竹谷豊 : 食餌性リン負荷が高齢期の脳に及ぼす影響の検討, 第 24 回・第 25 回日本病態栄養学会年次学術集会, 2022年1月.
34.	山本詩織, 奥村仙示, 大浦まゆ, 津村綾里, 川上葉奈, 多々納浩, 大南博和, 増田真志, 竹谷豊 : 日本食品成分表を用いた魚介類・肉類・豆類・卵類のアミノ酸と脂肪酸についての特徴の比較, 第 54 回日本栄養・食糧学会中国・四国支部大会/第 7 回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
35.	野邊悠太郎, 増田真志, 足立雄一郎, 山本菜摘, 大南博和, 奥村仙示, 竹谷豊 : 小胞体ストレスによる腸管リン酸輸送担体 Npt2b 発現調節機構の解明, 第 54 回日本栄養・食糧学会中国・四国支部大会/第 7 回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
36.	津村綾里, 奥村仙示, 川上葉奈, 大浦まゆ, 山本詩織, 大南博和, 増田真志, 竹谷豊 : 糖尿病食事療法のための食品交換表(第 2 版)を活用したアミノ酸・脂肪酸の調査, 第 54 回日本栄養・食糧学会中国・四国支部大会/第 7 回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
37.	滝川真輝, 大南博和, 北村彩乃, 國廣みなみ, 近藤睦珠, 松原未奈, 増田真志, 奥村仙示, 竹谷豊 : スクロースとリノール酸の組み合せは筋肉脂肪を増加させる, 第 54 回日本栄養・食糧学会中国・四国支部大会/第7 回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
38.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 大南博和, 奥村仙示, 二川健, 竹谷豊 : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の転写・転写後制御を介して筋繊維タイプ変化を引き起こす, 第 62 回日本生化学会中国・四国支部例会, 2021年9月.
39.	大浦まゆ, 奥村仙示, 平山明由, 川上葉奈, 多々納浩, 森根裕二, 大南博和, 増田真志, 島田光生, 曽我朋義, 冨田勝, 竹谷豊 : メタボローム解析を用いた肝切除術による肝臓のアミノ酸代謝物の変化, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, 2021年8月.
40.	津村綾里, 奥村仙示, 川上葉奈, 山本詩織, 大浦まゆ, 大南博和, 増田真志, 竹谷豊 : 糖尿病食事療法のための食品交換表活用編(第 2 版)におけるアミノ酸，脂肪酸の調査, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, 2021年8月.
41.	奥村仙示, 深来日菜, 川上葉奈, 津村綾里, 大南博和, 増田真志, 竹谷豊 : シームレスな食事指導のための献立のカロリー密度調査, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, 2021年8月.
42.	亀井優輝, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 成長期における血管石灰化抑制機構の解明, 第 75 回日本栄養・食糧学会大会, 2021年7月.
43.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 佐々木皓平, 野邊悠太郎, 大南博和, 大西康太, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の発現制御を介して筋繊維タイプ変化を誘導する, 第 75 回日本栄養・食糧学会大会, 2021年7月.
44.	山本詩織, 奥村仙示, 大浦まゆ, 津村綾里, 川上葉奈, 多々納浩, 大南博和, 増田真志, 竹谷豊 : 日本食品成分表2020年版(八訂)を用いた魚介類・肉類・豆類・卵類のアミノ酸と脂肪酸の比較, 第75回日本栄養・食糧学会大会, 2021年7月.
45.	大浦まゆ, 奥村仙示, 平山明由, 川上葉奈, 多々納浩, 森根裕二, 大南博和, 増田真志, 島田光生, 曽我朋義, 冨田勝, 竹谷豊 : メタボローム解析を用いた肝切除術による肝臓の代謝物変化の検討, 第75回日本栄養・食糧学会大会, 2021年7月.
46.	奥村仙示, 深来日菜, 川上葉奈, 津村綾里, 吉成春菜, 多々納浩, 大南博和, 増田真志, 竹谷豊 : 食べかたのコツ(Densiet)を数値化するための主食・主菜・副菜・間食献立に関するカロリー密度解析, 第75回日本栄養・食糧学会大会, 2021年7月.
47.	大南博和, 北村彩乃, 山口未来, 滝川真輝, 大西康太, 増田真志, 奥村仙示, 伊勢孝之, 八木秀介, 福田大受, 山田博胤, 佐田政隆, 竹谷豊 : 心不全マウスを用いた心リハ評価系の確立, 第27回日本心臓リハビテーション学会, 2021年6月.
48.	佐々木皓平, 増田真志, 足立雄一郎, 森優樹, 野邊悠太郎, 大南博和, 大西康太, 奥村仙示, 山本浩範, 竹谷豊 : 慢性腎臓病における all trans retinoic acid 水酸化酵素 Cyp26b1 制御機構の解明, 日本ビタミン学会第 73 回大会 Part1, 2021年6月.
49.	増田真志, 山本浩範, 武田英二, 竹谷豊 : 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, 2020年12月.
50.	坂井麻衣子, 大西康太, 春本恵里花, 増田真志, 大南博和, 奥村仙示, 板倉英祐, 原太一, 竹谷豊 : イソラムネチンによるエンドソーム成熟過程の亢進を介した異常分子除去作用, 2020年度日本フードファクター学会・日本農芸化学会西日本支部合同大会第332回講演会, 2020年11月.
51.	佐々木晧平, 増田真志, 足立雄一郎, 大西康太, 大南博和, 奥村仙示, 竹谷豊 : 慢性腎臓病におけるAll-trans retinoic acid (ATRA) 水酸化酵素Cyp26b1制御機構の解明, 第53回日本栄養・食糧学会中国・四国支部大会, 2020年10月.
52.	木村玲奈, 増田真志, 野邊悠太郎, 大西康太, 大南博和, 奥村仙示, 竹谷豊 : 食餌性リン負荷は高齢マウスの脳内ATP量を減少させる, 第53回日本栄養・食糧学会中国・四国支部大会, 2020年10月.
53.	佐守美穂, 亀井優輝, 大西康太, 足立雄一郎, 増田真志, 大南博和, 奥村仙示, 竹谷豊, 羽田尚彦, 井上淳詞 : NSAIDs起因性小腸傷害に対するほうれん草由来グリセロ糖脂質の影響, 第53回日本栄養・食糧学会中国・四国支部大会, 2020年10月.
54.	奥村陽介, 酒井晶子, 阿部航太郎, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 慢性腎臓病に伴う亜鉛代謝異常の発症機序解明, 第53回日本栄養・食糧学会中国・四国支部大会, 2020年10月.
55.	増田真志, 山本浩範, 竹谷豊 : All-trans retinoic acidは腸管II型ナトリウム依存性リン酸輸送担体(Npt2b)遺伝子発現を低下させる, 第22回日本骨粗鬆症学会/ 第38回日本骨代謝学会学術集会, 2020年10月.
56.	小松原彩乃, 岸本麻希, 多々納(福田) 詩織, 林眞由, 江原みゆ, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 妊娠前の高リン食摂取は，仔マウスの食後血中リン濃度上昇を亢進させる, 第74回日本栄養・食糧学会大会, 2020年9月.
57.	坂井麻衣子, 大西康太, 増田真志, 大南博和, 奥村仙示, 板倉英祐, 原太一, 竹谷豊 : MΦにおける異常タンパク質分解を促進するイソラムネチンの作用機序解析, 日本農芸化学会2020年度中四国支部大会, 2020年9月.
58.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 妊娠前の食餌性リン負荷が，仔マウスのリン応答性に及ぼす影響, 第93回日本生化学会大会, 2020年9月.
59.	石谷さとの, 新居紗知, 楢﨑遥子, 奥村仙示, 山本浩範, 増田真志, 大西康太, 大南博和, 竹谷豊 : 幹細胞における組織非特異的アルカリフォスファターゼ遺伝子発現とリン代謝に対するSNPrs1697421, 第93回日本生化学会大会, 2020年9月.
60.	福田詩織, 山本浩範, 中橋乙起, 増田真志, 竹谷豊 : 成長期における過剰な食餌性リン摂取時のカルシウム摂取量の違いがα-klotho発現に及ぼす影響, 第67回日本栄養改善学会学術集会, 2020年9月.
61.	山本浩範, 田尻真梨, 中橋乙起, 増田真志, 大南博和, 大西康太, 石黒真理子, 池田涼子, 岩野正之, 武田英二, 竹谷豊 : 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, 2020年9月.
62.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 妊娠前の食餌性リン負荷は，成熟仔マウスのリン応答性を攪乱する, 第67回日本栄養改善学会学術集会, 2020年9月.
63.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 妊娠前の食餌性リン負荷が，仔マウスのリン応答性に及ぼす影響, 第61回日本生化学会中国四国支部例会, 2020年7月.
64.	亀井優輝, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 小児期における血中リン濃度とFetuin-Aとの関係, 第61回日本生化学会中国四国支部例会, 2020年7月.
65.	足立雄一郎, 増田真志, 大西康太, 大南博和, 奥村仙示, 竹谷豊 : 慢性腎臓病におけるビタミンA代謝異常が転写因子XBP1に及ぼす影響, 第61回日本生化学会中国四国支部例会, 2020年7月.
66.	山本浩範, 石黒真理子, 田中更沙, 竹井悠一郎, 増田真志, 大西康太, 竹谷豊 : 生体ビタミンD作用に及ぼすファイトケミカルの影響, 日本ビタミン学会第72回大会, 2020年6月.
67.	森優樹, 増田真志, 吉田里沙, 青柳咲紀, 大西康太, 大南博和, 奥村仙示, 山本浩範, 濱田広一郎, 竹谷豊 : レチノイン酸によるオートファジーを介した脂肪分解への影響, 日本ビタミン学会第72回大会, 2020年6月.
68.	山本浩範, 田尻真梨, 中橋乙起, 増田真志, 大南博和, 大西康太, 武田英二, 竹谷豊 : 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74回日本栄養・食糧学会大会, 2020年4月. (キーワード) ビタミンD (vitamin D) / カルシウム (calcium) / 糖尿病 (diabetes)
69.	坂井麻衣子, 大西康太, 増田真志, 大南博和, 奥村仙示, 原太一, 竹谷豊 : 栄養素応答シグナルmTORC2を介したリソソーム活性制御機構の解明, 第74回日本栄養・食糧学会大会, 2020年4月. (キーワード) リソソーム / mTORC2 / マクロファージ (macrophage)
70.	徳里望, 阪上浩, 堤理恵, 黒田雅士, 升本早枝子, 武田英二, 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, 片山貴文, 堤理恵, 阪上浩, 竹谷豊 : 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, ビタミン, Vol.94, No.4, 277, 2020年4月. (キーワード) 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
71.	福田哲平, 大西康太, 増田真志, 松崎泰教, 今野歩, 藤元萌, 大西愛花, 坂井麻衣子, 大南博和, 奥村仙示, 原太一, 平井宏和, 竹谷豊 : 近赤外蛍光イメージングを用いたin vivoオートファジー活性評価法の構築, 日本農芸化学会2020年度大会, 2020年3月. (キーワード) オートファジー (autophagy) / 近赤外蛍光イメージング / アデノ随伴ウィルスベクター
72.	坂井麻衣子, 大西康太, 増田真志, 大南博和, 奥村仙示, 原太一, 竹谷豊 : J774.1マクロファージ様細胞においてmTORC2シグナルはリソソーム活性を制御する, 日本農芸化学会2020年度大会, 2020年3月. (キーワード) リソソーム / マクロファージ (macrophage) / mTORC2
73.	池田美萌, 織田奈央子, 上番増喬, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 高リン食が腸内環境を介して慢性腎臓病に与える影響, 第23回日本病態栄養学会年次集会, 2020年1月.
74.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病による骨格筋の脂肪酸代謝異常を介した脂肪毒性(Liptoxicity)は筋委縮(サルコペニア) を惹起する, 第23回日本病態栄養学会年次集会, 2020年1月.
75.	亀井優輝, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 小児期において血中 Fetuin-A 濃度とリン濃度は相関する, 第52回日本栄養・食糧学会中国・四国支部会, 2019年10月.
76.	森優樹, 増田真志, 吉田里沙, 青柳咲紀, 大西康太, 大南博和, 奥村仙示, 二川健, 濱田広一郎, 竹谷豊 : レチノイン酸によるリポファジーを介した脂肪分解への影響, 第52回日本栄養・食糧学会中国•四国支部大会, 2019年10月.
77.	坂井麻衣子, 大西康太, 大南博和, 増田真志, 奥村仙示, 竹谷豊 : mTORC2シグナルはマクロファージ様細胞において遺伝子発現調節を介してリソソーム活性を制御する, 第92回日本生化学会大会, 2019年9月.
78.	山本浩範, 石黒真理子, 竹井悠一郎, 中橋乙起, 増田真志, 竹谷豊, 岩野正之 : 食餌性リンはNuclear factor-E2-related factor 2を介し酸化ストレス応答・解毒関連遺伝子の発現を調節する, 第66回日本栄養改善学会学術集会, 2019年9月.
79.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病モデルラットの骨格筋における脂肪酸代謝異常が及ぼす筋萎縮への影響, 第66回日本栄養改善学会学術集会, 2019年9月.
80.	佐藤景子, 増田真志, 佐々木晧平, 大南博和, 大西康太, 奥村仙示, 山本浩範, 竹谷豊 : All-trans retinoic acidによるヒストン修飾を介したFGF23発現への影響, 第7回日本腎栄養代謝研究会, 2019年7月.
81.	福田詩織, 山本浩範, 中橋乙起, 吉川亮平, 林眞由, 岸本麻希, 伊美友紀子, 奥村仙示, 増田真志, 大西康太, 竹谷豊 : 成長期における短期的・長期的食餌性リン負荷がFGF23/α-klothoシグナルに及ぼす影響, 日本ビタミン学会第71回大会, 2019年6月.
82.	山本浩範, 中尾真理, 中橋乙起, 増田真志, 竹谷豊 : リン制限による鉄代謝および腎性貧血への影響, 日本ビタミン学会第71回大会, 2019年6月.
83.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : レチノイン酸による小胞体ストレス感受性の影響, 日本ビタミン学会第71回大会, 2019年6月.
84.	岸本麻希, 福田詩織, 林眞由, 増田真志, 竹谷豊 : 妊娠期の高リン食摂取が仔の発育やリン代謝調節系に及ぼす影響, 第73回日本栄養・食糧学会大会, 2019年5月.
85.	香川知博, 山本浩範, 中橋乙起, 原田永勝, 増田真志, 武田英二, 竹谷豊 : 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, 2019年5月.
86.	佐藤景子, 増田真志, 足立雄一郎, 大西康太, 奥村仙示, 山本浩範, 竹谷豊 : All-trans retinoic acidによるヒストン修飾を介したFGF23発現への影響, 第73回日本栄養・食糧学会大会, 2019年5月.
87.	藤元萌, 大西康太, 坂井麻衣子, 福田哲平, 大西愛花, 増田真志, 奥村仙示, 河合慶親, 竹谷豊 : オートファジー活性を制御する食品成分の探索, 日本農芸化学会2019年度大会, 2019年3月. (キーワード) オートファジー (autophagy) / 食品成分
88.	吉澤和香, 中尾真理, 伊美友紀子, 矢引紀江, 新井田裕樹, 増田真志, 奥村仙示, 竹谷豊 : 慢性腎臓病に伴う骨ミネラル代謝異常(CKD-MBD)における骨ー筋連関, 第22回日本病態栄養学会年次学術集会(パシフィコ横浜), 2019年1月.
89.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 二川健, 竹谷豊 : 小胞体ストレス誘導下におけるレチノイン酸の影響, 第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月.
90.	新居紗知, 勝本美咲, 楢﨑遥子, 世古千裕, 山﨑通世, 奥村仙示, 山本浩範, 武田英二, 竹谷豊 : 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), 2018年9月.
91.	吉田里沙, 増田真志, 森優樹, 新井田裕樹, 足立雄一郎, 大西康太, 河合慶親, 二川健, 山本浩範, 竹谷豊 : スルフォラファンのリポファジーを介した脂肪分解効果, Food Congress 2018, 2018年9月.
92.	林眞由, 福田詩織, 竹谷豊, 山本浩範 : 妊娠前における食餌性リン負荷が新生仔マウスのリン代謝調節系に及ぼす影響, 第36回日本骨代謝学会学術集会(長崎ブリックホール), 2018年7月.
93.	山本浩範, 福田詩織, 増田真志, 竹井悠一郎, 竹谷豊 : 食餌性リンはNuclear factor-E2-related factor 2を介し酸化ストレス応答・解毒関連遺伝子の発現を調節する, 第36回日本骨代謝学会学術集会(長崎ブリックホール), 2018年7月.
94.	竹谷豊, 伊美友紀子, 増田真志, 山本浩範 : リン過剰摂取の病態栄養学, 第36回日本骨代謝学会学術集会(長崎ブリックホール), 2018年7月.
95.	甲谷芹奈, 増田真志, イリムラティイマム, 奥村仙示, 山本浩範, 竹谷豊 : 慢性腎臓病における鉄代謝異常に対するレチノイン酸の影響, 日本ビタミン学会第70回大会(高槻現代劇場), 2018年6月.
96.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 内田貴之, 大西康太, 河合慶親, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病に伴う骨格筋の飽和脂肪酸蓄積はオートファジー不全を介して筋萎縮を誘発する, 日本ビタミン学会第70回大会(高槻現代劇場), 2018年6月.
97.	林眞由, 福田詩織, 岸本麻希, 増田真志, 竹谷豊 : 妊娠前におけるリン過剰摂取が新生仔マウスのリン代謝調節系を撹乱する, 第59回日本生化学会中国・四国支部例会(米子市文化ホール), 2018年5月.
98.	吉田里沙, 新井田裕樹, 足立雄一郎, 酒井晶子, 奥村仙示, 大西康太, 内田貴之, 河合慶親, 山本浩範, 二川健, 竹谷豊, 増田真志 : スルフォラファンのリポファジーを介した脂肪分解効果, 第72回日本栄養・食糧学会大会(岡山県立大学), 2018年5月.
99.	林眞由, 福田詩織, 岸本麻希, 増田真志, 奥村仙示, 竹谷豊 : 妊娠前における食餌性リン負荷が新生仔マウスのリン代謝調節系に及ぼす影響, 第72回日本栄養・食糧学会大会(岡山県立大学), 2018年5月.
100.	竹谷豊, 木藤有紀, 伊美友紀子, 奥村仙示, 増田真志 : 2.副甲状腺ホルモン初期分泌機構とその役割 (脂溶性ビタミン総合研究委員会・第353回会議研究発表要旨), ビタミン, Vol.91, No.3, 208, 2018年. (出版サイトへのリンク) ● Publication site (DOI): 10.20632/vso.91.3_208 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680809733632 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.91.3_208 (DOI: 10.20632/vso.91.3_208, CiNii: 1390282680809733632)
101.	酒井晶子, 阿部航太郎, 伊美友紀子, Yilimurati Yimamu, 竹内綾乃, 増田真志, 奥村仙示, 神戸大朋, 山本浩範, 竹谷豊 : 慢性腎臓病における亜鉛代謝異常と亜鉛補充食の効果, 第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月.
102.	甲谷芹奈, 増田真志, 新井田裕樹, 足立雄一郎, 山田あかり, 奥村仙示, 竹谷豊 : 慢性腎臓病におけるレチノイン酸の腎性貧血に対する影響, 第50回日本栄養・食糧学会中国四国支部大会, 2017年11月.
103.	吉田里沙, 増田真志, 青柳咲紀, 伊美友紀子, イリムラティイマム, 奥村仙示, 竹谷豊 : 肥満に対するスルフォラファンの影響, 第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月.
104.	多々納浩, 奥村仙示, 穂満史子, 増田真志, 竹谷豊 : メタボローム解析による肉及び魚摂取バイオマーカーの探索, 第64回日本栄養改善学会学術総会, 2017年9月.
105.	穂満史子, 奥村仙示, 多々納浩, 増田真志, 竹谷豊 : メタボロミクスによる飲料摂取バイオマーカーの探索, 第64回日本栄養改善学会学術総会, 2017年9月.
106.	福田詩織, 山本浩範, 中橋乙起, 増田真志, 竹谷豊 : 成長期における食餌性リンによるα-klotho発現制御, 第64回日本栄養改善学会学術総会, 2017年9月.
107.	新井田裕樹, 増田真志, 足立雄一郎, イマムイリムラティ, 奥村仙示, 山本浩範, 竹谷豊 : 骨格筋脂質代謝異常が慢性腎臓病に伴う尿毒症性サルコペニア(筋委縮)を誘発する, 第64回日本栄養改善学会学術総会, 2017年9月.
108.	山口智勢, 奥村仙示, 多々納浩, 井端知咲, 藤岡真理子, 窪田友華, 近藤知佳, 多々納浩, 竹谷豊 : デンシエット(Densiet)によるカロリー密度(CD)に注目した低カロリー満腹食の開発, 第64回日本栄養改善学会, 2017年9月.
109.	吾妻雅彦, 長宗雅美, 岩田貴, 川添和義, 石澤啓介, 竹谷豊, 西岡安彦, 赤池雅史 : 徳島大学における担当患者を用いた多職種連携教育の取り組み, 第49回日本医学教育学会大会, 2017年8月.
110.	竹谷豊, 楢﨑遙子, 奥村仙示, 増田真志 : 食事性リンとリン負荷指数, 第62回日本透析医学会学術集会・総会, 2017年6月.
111.	山本浩範, 香川知博, 中橋乙起, 石黒真理子, 増田真志, 武田英二, 竹谷豊 : 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, 2017年6月.
112.	伊美友紀子, 矢引紀江, Abuduli Maerjianghan, 増田真志, 奥村仙示, 竹谷豊 : 高リン食による白色脂肪組織量の減少, 日本ビタミン学会第69回大会, 2017年6月.
113.	竹谷豊, 福田詩織, 奥村仙示, 増田真志 : リンと心血管疾患:リン制限は寿命を延伸する?, 第17回日本抗加齢医学会総会, 2017年6月.
114.	新井田祐樹, 増田真志, 吉澤和香, Yimamu Ilimulati, 吉田里沙, 甲谷芹奈, 奥村仙示, 河合慶親, 竹谷豊, 山本浩範 : 骨格筋脂質代謝異常が慢性腎臓病に伴うProtein Energy Wasting (CKD-PEW) を誘発する, 第71回日本栄養・食糧学会大会, 2017年5月.
115.	織田奈央子, 杉原康平, 吉本亜由美, 上番増喬, 増田真志, 奥村仙示, 竹谷豊 : 高リン食摂取は腸内環境を変化させる, 日本栄養食糧学会, 322, 2017年5月.
116.	竹内綾乃, 石田陽子, 増田真志, 竹谷豊, 羽田尚彦, 小笠原明恵, 奥村仙示 : 抗がん剤誘発性の悪心・嘔吐に対するホウレンソウ由来グリセロ糖脂質の抑制効果, 第71回日本栄養・食糧学会大会, 2017年5月.
117.	竹内綾乃, 石田陽子, 羽田尚彦, 小河原明恵, 増田真志, 奥村仙示, 竹谷豊 : 抗がん剤誘発性の悪心・嘔吐に対するホウレンソウ由来グリセロ糖脂質の抑制効果, 日本病態栄養学会年次学術集会, 2017年1月.
118.	山口智勢, 奥村仙示, 江角遥佳, 増田真志, 竹谷豊 : 血糖値・血清インスリン濃度及び嗜好性に影響を与える脂質負荷量の検討, 日本病態栄養学会年次学術集会, 2017年1月.
119.	新井田裕樹, 増田真志, 吉澤和香, 奥村仙示, 竹谷豊 : 慢性腎臓病に伴う脂質代謝異常がProtein Eneregy Wastingに与える影響, 日本栄養・食糧学会中国・四国支部大会, 2016年11月.
120.	山口智勢, 奥村仙示, 江角遥佳, 増田真志, 竹谷豊 : 生体や嗜好性に影響を与える脂質負荷量の検討, 日本栄養・食糧学会中国・四国支部, 2016年11月.
121.	多々納浩, 奥村仙示, 梶浦大資, 近藤千佳, 平山明由, 馬渡一諭, 河合慶親, 増田真志, 竹谷豊 : GC-MSを用いた肉の種類別の摂取バイオマーカーの探索, 第10回メタボロームシンポジウム, 2016年10月.
122.	竹谷豊, 楢崎遥子, 山本浩範 : 食事性リンとリン負荷指数, 第34回日本骨代謝学会学術集会, 2016年7月.
123.	矢引紀江, 伊美友紀子, Abuduli Maerjianghan, 増田真志, 奥村仙示, 山本浩範, 武田英二, 竹谷豊 : 高脂肪食が高リン食摂取時のミネラル代謝調節機構に及ぼす影響, 日本ビタミン学会第68回大会, 2016年6月.
124.	山本浩範, 吉川亮平, 福田詩織, 中橋乙起, 石黒真理子, 増田真志, 武田英二, 竹谷豊 : α-klotho発現およびビタミンD代謝に及ぼす加齢と食餌性リンの影響, 日本ビタミン学会第68回大会, 2016年6月.
125.	山本浩範, 岡村友理香, 石黒真理子, 中橋乙起, 青木菜摘, 柴田重信, 岩野正之, 竹谷豊 : ビタミンD代謝の概日リズムの分子機構の解明と時間治療への応用, 第70回日本栄養・食糧学会大会, 2016年5月.
126.	杉原康平, 増田真志, 中尾真理, Abuduli Maerjianghan, 石田陽子, 山本浩範, 武田英二, 竹谷豊 : 食事性リンが炎症性腸疾患の病態および腸管バリア機能に及ぼす影響, 第70回日本栄養・食糧学会大会, 2016年5月.
127.	川本桂祐, 佐久間理英, 田中更沙, 増田真志, 中尾真理, 新井田裕樹, 伊藤美紀子, 竹谷豊, 新井英一 : 糖質・脂質の組成比率がリン代謝動態に及ぼす影響, 第70回日本栄養・食糧学会大会, 2016年5月.
128.	石田陽子, 竹内綾乃, 増田真志, 奥村仙示, 羽田尚彦, 竹谷豊 : 5-FU誘導性腸粘膜障害に対するホウレンソウ由来グリセロ糖脂質の防御効果, 第70回日本栄養・食糧学会大会, 2016年5月.
129.	楢崎遥子, 勝本美咲, 中川倫美, 松野真実, 野田恒行, 奥村仙示, 竹谷豊 : 長期的なリン利尿調節因子FGF-23を指標としたリン負荷指数の妥当性の検討, 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, 2016年1月.
130.	杉原康平, 増田真志, 中尾真理, Abuduli Maerjianghan, 石田陽子, 山本浩範, 武田英二, 竹谷豊 : 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, 2016年1月.
131.	Abuduli Maerjianghan, 大南博和, 阪上浩, 大谷環樹, 上田遥香, 武田英二, 竹谷豊 : 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, 2015年10月.
132.	和田宵湖, 奥村仙示, 竹谷豊, 松村晃子 : 肝癌患者における重症度及び肝切除量の違いによる肝切除前後のエネルギー代謝へ及ぼす影響評価, 第62回日本栄養改善学会学術総会，福岡国際会議場，福岡県福岡市，2015年9月24日~26日, 2015年9月.
133.	楢崎遥子, 勝本美咲, 奥村仙示, 竹谷豊 : FGF-23を指標としたリン負荷指数の妥当性の検討, 第62回日本栄養改善学会学術総会，福岡国際会議場，福岡県福岡市，2015年9月24日~26日, 2015年9月.
134.	多々納浩, 奥村仙示, 竹谷豊 : デンシエット弁当を用いた，脂質摂取の多い食習慣が嗜好性へ及ぼす影響についての検討, 第62回日本栄養改善学会学術総会，福岡国際会議場，福岡県福岡市，2015年9月24日~26日, 2015年9月.
135.	中橋乙起, 山本浩範, 田中更沙, 竹谷豊 : マウスにおいて短期間の食餌性リン制限は回腸Fibroblast growth factor 15遺伝子発現量を増加させる, 第62回日本栄養改善学会学術総会，福岡国際会議場，福岡県福岡市，2015年9月24日~26日, 2015年9月.
136.	石田陽子, 竹谷豊, 羽田尚彦 : 5-FU誘導性腸粘膜障害に対するホウレンソウ由来グリセロ糖脂質の防御効果, 第62回日本栄養改善学会学術総会，福岡国際会議場，福岡県福岡市，2015年9月24日~26日, 2015年9月.
137.	多々納浩, 奥村仙示, 竹谷豊, 増田真志 : 生活習慣病の要:栄養教育と実践, 第62回日本栄養改善学会学術総会, 2015年9月.
138.	梶浦大資, 奥村仙示, 竹谷豊, 片山貴文, 松村晃子, 島田光生, 平山明由, 冨田勝, 曽我朋義 : 肝癌患者における肝切除前・後の血清及び尿中メタボローム解析, 第251回徳島医学会, 2015年8月.
139.	中尾真理, 山本浩範, 福田詩織, 竹谷豊, 武田英二 : 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, 2015年7月.
140.	福田詩織, 山本浩範, 中尾真理, 武田英二, 竹谷豊 : 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, 2015年7月.
141.	木藤有紀, 阿部航太郎, 中尾真理, 大西里奈, 伊美友紀子, 石田陽子, 矢引紀江, 大南博和, 奥村仙示, 竹谷豊 : 食事性リン摂取による副甲状腺ホルモン初期分泌機構の解明, 第58回日本腎臓学会学術総会，名古屋国際会議場，愛知県名古屋市，2015年6月5日~7日, 2015年6月.
142.	山本浩範, 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, 竹谷豊, 武田英二 : 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, 2015年6月.
143.	中尾真理, 山本浩範, 中橋乙起, 池田翔子, 阿部航太郎, 福田詩織, 武田英二, 竹谷豊 : 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, 2015年6月.
144.	福田詩織, 山本浩範, 中橋乙起, 池田翔子, 中尾真理, 横山望, 吉川亮平, 大西里奈, 武田英二, 竹谷豊 : 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, 2015年6月.
145.	和田宵湖, 奥村仙示, 武田英二, 竹谷豊, 片山貴文, 荒川悠佑, 居村暁, 島田光生 : 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, 2015年4月.
146.	和田宵湖, 奥村仙示, 杉原康平, 山本モモ, 竹谷豊, 島田光生, 武田英二 : 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, 2015年1月.
147.	多々納浩, 奥村仙示, 周蓓, 片山貴文, 竹谷豊, 武田英二 : 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, 2015年1月.
148.	楢﨑遥子, 竹谷豊, 松浦明香, 森西真由美, 米田武志, 山崎通世, 勝本美咲, 濵田康弘, 武田英二 : 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, 2015年1月.
149.	勝本美咲, 竹谷豊, 山崎通世, 奥村仙示, 山本浩範, 武田英二 : 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, 2015年1月.
150.	杉原康平, 奥村仙示, 和田宵湖, 山本モモ, 竹谷豊, 山田眞一郎, 居村暁, 島田光生, 武田英二 : 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, 2015年1月.
151.	伊美友紀子, 竹谷豊, Maerjianghan Abuduli, 矢引紀江, 谷口由莉, 大南博和, 武田英二 : 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, 2014年10月.
152.	谷口由莉, 竹谷豊, 大南博和, Maerjianghan Abuduli, 伊美友紀子, 坂田ひろみ, 山本浩範, 武田英二 : 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, 2014年10月.
153.	小林謙一, 志賀孝宏, 滝拓也, 石井京子, 石田香織, 河田哲典, 瀬川博子, 宮本賢一, 竹谷豊, 田所忠弘, 松井芳光, 山本祐司 : ビタミンB12欠乏が腎臓におけるビタミンDや無機リンの再吸収に及ぼす影響, 第87回日本生化学会大会，平成26年10月15日—10月18日，国立京都国際会館, 2014年10月.
154.	竹谷豊 : リン代謝調節機構の破綻と心血管疾患, 第26回腎とフリーラジカル研究会シンポジウム「臨床への展開を目指した基礎研究からの情報発信」平成26年9月20日，ウインクあいち，名古屋, 2014年9月.
155.	竹谷豊 : 徳島大学医科栄養学科における臨床栄養学教育の展望, 第3回日本栄養学教育学会ワークショップ，平成26年8月23日神奈川県立保健福祉大学, 2014年8月.
156.	奥村仙示, 足立知咲, 松村晃子, 竹谷豊, 武田英二 : 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, 2014年8月.
157.	勝本美咲, 竹谷豊, 奥村仙示 : CKD患者におけるリン制御指導のためのリン生体利用率評価法の確立, 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, 2014年8月.
158.	山本浩範, 大西里奈, 福田詩織, 竹井悠一郎, 竹谷豊, 武田英二 : 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, 2014年7月.
159.	松浦明香, 竹谷豊, 森西真由美, 米田武志, 山崎通世, 勝本美咲, 濵田康弘, 武田英二 : 食品中リンの生体利用率の評価, 第57回日本腎臓学会, 2014年7月.
160.	松浦明香, 竹谷豊, 森西真由美, 米田武志, 山崎通世, 勝本美咲, 濵田康弘, 武田英二 : 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, 2014年6月.
161.	竹谷豊, 松浦明香, 森西真由美, 米田武志, 山崎通世, 勝本美咲, 濵田康弘, 武田英二 : 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, 2014年6月.
162.	竹谷豊, 森西真由美, 松浦明香, 米田武志, 山崎通世, 勝本美咲, 濵田康弘, 奥村仙示, 武田英二 : 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, 2014年6月.
163.	山本浩範, 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, 竹谷豊, 武田英二 : 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, 2014年6月.
164.	福田詩織, 山本浩範, 中橋乙起, 池田翔子, 横山望, 吉川亮平, 大西里奈, 竹谷豊, 武田英二 : 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, 2014年5月.
165.	多々納浩, 奥村仙示, 周蓓, 竹谷豊, 武田英二 : 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, 2014年5月.
166.	多々納浩, 奥村仙示, 周蓓, 竹谷豊, 武田英二 : 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, 2014年5月.
167.	竹谷豊 : 第17回日本病態栄養学会(シンポジウム)，大阪，1月11日~12日，2014年, 2014年1月.
168.	竹谷豊 : Emerging roles of sodium-dependent phosphate transporters in mineral metabolism, diseases and beyond., 日本薬物動態学会第28回年会(シンポジウム)，東京，10月9日~11日，2013年, 2013年10月.
169.	山崎通世, 勝本美咲, 竹谷豊, 奥村仙示 : 食後血糖上昇および糖代謝調節ホルモンに対して食事性リンが及ぼす影響, 第60回日本栄養改善学会学術総会，神戸，9月12日~14日，2013年, 2013年9月.
170.	竹谷豊, 山本浩範, 奥村仙示, 武田英二 : 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, 2013年6月.
171.	吉川亮平, 山本浩範, 香川知博, 中橋乙起, 横山望, 大西里奈, 池田翔子, 竹谷豊, 武田英二 : 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, 2013年5月.
172.	中尾真理, 山本浩範, 阿部航太郎, 中橋乙起, 池田翔子, 竹谷豊, 武田英二 : 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, 2013年5月.
173.	山本浩範, 香西美奈, 香川知博, 原田永勝, 中橋乙起, 池田翔子, 竹谷豊, 武田英二 : 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, 2013年5月.
174.	香川知博, 山本浩範, 香西美奈, 原田永勝, 向原理恵, 竹谷豊, 武田英二 : 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, 2013年5月.
175.	山本浩範, 田尻真梨, 中橋乙起, 香西美奈, 香川知博, 竹谷豊, 武田英二 : 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, 2013年5月.
176.	山本浩範, 香西美奈, 香川知博, 竹谷豊, 武田英二 : 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, 2013年5月.
177.	田尻真梨, 山本浩範, 中橋乙起, 香川知博, 竹谷豊, 佐々木一, 武田英二 : 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, 2013年1月.
178.	竹谷豊 : 腎疾患におけるリン・タンパク質, 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, 2013年1月.
179.	Maerjianghan Abduli, 竹谷豊, 大南博和, 上田遙香, 谷口由莉, 山本浩範, 武田英二 : 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), 肥満研究, Vol.18, No.Supplement, 175, 2012年9月.
180.	武田英二, 奥村仙示, 山本浩範, 竹谷豊 : 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, 2012年9月.
181.	山本浩範, 向原理恵, 中橋乙起, 池田翔子, 香西美奈, 竹谷豊, 武田英二 : 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, 2012年7月.
182.	山本浩範, 大谷彩子, 横山望, 香西美奈, 池田翔子, 竹谷豊, 武田英二 : 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, 2012年7月.
183.	武田英二, 山本浩範, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 冨永辰也, 土井俊夫 : 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), ビタミン, Vol.86, No.5, 358-359, 2012年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680677126528 (CiNii: 1390282680677126528)
184.	武田英二, 山本浩範, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 冨永辰也, 土井俊夫 : 局所的CYP27B1発現亢進による異所性石灰化, ビタミン, Vol.86, No.5-6, 358-359, 2012年6月.
185.	向原理恵, 山本浩範, 中橋乙起, 池田翔子, 香西美奈, 竹谷豊, 武田英二 : 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), ビタミン, Vol.86, No.4, 244, 2012年4月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680761309824 (CiNii: 1390282680761309824)
186.	上田遙香, アブドリマルジャンハン, 山本浩範, 竹谷豊, 武田英二 : 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), 日本腎臓学会誌, Vol.54, No.3, 321, 2012年4月.
187.	大南博和, Wanjihia Violet, 竹谷豊, 奥村仙示, 山本浩範, 武田英二 : 肝臓の脂質代謝を制御する胎生期栄養環境(会議録), 糖尿病, Vol.55, No.Supplement.1, S336, 2012年4月.
188.	十河未来, 山本浩範, 香西美奈, 池田翔子, 中橋乙起, 大谷彩子, 竹谷豊, 武田英二 : 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, 2012年4月.
189.	中尾真理, 山本浩範, 中橋乙起, 池田翔子, 香西美奈, 田中更沙, 竹谷豊, 武田英二 : 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, 2012年4月.
190.	森本優香, 佐久間理英, 太田紘之, 梅田見名子, 石川真, 竹谷豊, 武田英二, 新井英一 : 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, 2012年4月.
191.	山本浩範, 増田真志, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 : 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, 2012年4月.
192.	大谷彩子, 山本浩範, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 冨永辰也, 土井俊夫, 武田英二 : 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, 2012年2月.
193.	中尾真理, 山本浩範, 中橋乙起, 池田翔子, 香西美奈, 田中更沙, 竹谷豊, 武田英二 : 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, 2012年1月.
194.	大南博和, 阿望幾久子, 竹谷豊, 佐藤佳瑞智, 新井英一, 小金井恵, 佐々木一, 奥村仙示, 山本浩範, 武田英二 : 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, 2012年1月.
195.	向原理恵, 山本浩範, 中橋乙起, 池田翔子, 香西美奈, 竹谷豊, 武田英二 : 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, 2011年11月.
196.	武田英二, 山本浩範, 奥村仙示, 竹谷豊 : 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, 2011年10月.
197.	竹谷豊 : リン代謝恒常性の破綻と血管疾患, 第50回日本栄養・食糧学会近畿支部大会, 2011年10月.
198.	大南博和, Wanjihia Violet, 竹谷豊, 阿望幾久子, 奥村仙示, 山本浩範, 武田英二 : 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, 2011年9月.
199.	竹谷豊, 上番増喬, 大南博和, 武田英二 : 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, 2011年9月.
200.	堀江大輔, 山田歩規代, 谷村綾子, 竹谷豊, 山本浩範, 宮本賢一, 武田英二 : 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, 2011年9月.
201.	竹谷豊, 山本浩範, 奥村仙示, 宮本賢一, 武田英二 : 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, 2011年9月.
202.	竹谷豊, ヴヴァンタン, 宮本賢一, 山本浩範, 武田英二 : 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, 2011年7月.
203.	山本浩範, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 : 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, 2011年7月.
204.	山本浩範, 池田翔子, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 : 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, 2011年7月.
205.	竹谷豊 : リン代謝制御の破綻と疾患(若手シンポジウム「ビタミン・バイオファクター研究の最前線から」,日本ビタミン学会第63回大会講演要旨), ビタミン, Vol.85, No.4, 205-206, 2011年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205702188800 (CiNii: 1390001205702188800)
206.	山本浩範, 増田真志, 田中更紗, 香西美奈, 竹谷豊, 宮本賢一, 武田英二 : 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), ビタミン, Vol.85, No.4, 218, 2011年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205784275840 (CiNii: 1390001205784275840)
207.	大谷彩子, 山本浩範, 竹井悠一郎, 香西美奈, 竹谷豊, 武田英二 : 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), ビタミン, Vol.85, No.4, 254, 2011年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205784435712 (CiNii: 1390001205784435712)
208.	田中輝実, Van Vu Tan, 竹谷豊, 山本浩範, 武田英二 : 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, 2011年5月.
209.	中橋乙起, 山本浩範, 田中更沙, 向原理恵, 池田翔子, 橋本脩平, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2011年5月.
210.	山本浩範, 増田真志, 香西美奈, 中橋乙起, 池田翔子, 竹谷豊, 瀬川博子, 宮本賢一, 武田英二 : 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, 2011年5月.
211.	山本浩範, 菊地浩子, 中尾真理, 中橋乙起, 池田翔子, 田中更沙, 竹谷豊, 武田英二 : 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, 2011年1月.
212.	山本浩範, 香西美奈, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年12月.
213.	中橋乙起, 山本浩範, 田中更紗, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年11月.
214.	山本浩範, 菊地浩子, 中尾真理, 中橋乙起, 池田翔子, 田中更沙, 竹谷豊, 武田英二 : 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, 日本病態栄養学会誌, Vol.13, No.5, 165, 2010年11月. (キーワード) *腎不全(実験的)
215.	山本浩範, 香西美奈, 竹谷豊, 武田英二, 宮本賢一, 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), ビタミン, Vol.84, No.8, 408, 2010年8月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205701667456 (CiNii: 1390001205701667456)
216.	山本浩範, 香西美奈, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年7月.
217.	山本浩範, 竹井悠一郎, 佐藤匡俊, 竹谷豊, 武田英二 : 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, 2010年7月.
218.	山本浩範, 香西美奈, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年7月.
219.	中橋乙起, 山本浩範, 池田翔子, 田中更沙, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年6月.
220.	増田真志, 山本浩範, 香西美奈, 石黒真理子, 中橋乙起, 田中更沙, 竹谷豊, 宮本賢一, 武田英二 : 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, 2010年6月.
221.	山本浩範, 浦川千鶴, 香西美奈, 増田真志, 中橋乙起, 竹谷豊, 山本雅之, 武田英二 : 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, 2010年6月.
222.	大谷彩子, 山本浩範, 竹井悠一郎, 香西美奈, 竹谷豊, 武田英二 : 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, 2010年6月.
223.	阿望幾久子, 大南博和, 竹谷豊, 佐藤佳瑞智, 深谷牧子, 上番増喬, 新井英一, 小金井恵, 佐々木一, 山本浩範, 武田英二 : 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, 2010年5月.
224.	阿望幾久子, 大南博和, 竹谷豊, 佐藤佳瑞智, 深谷牧子, 上番増喬, 新井英一, 小金井恵, 佐々木一, 山本浩範, 武田英二 : 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, 2010年5月.
225.	大南博和, 阿望幾久子, 竹谷豊, 上番増喬, 佐藤佳瑞智, 深谷牧子, 新井英一, 小金井恵, 佐々木一, 山本浩範, 武田英二 : 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, 2010年5月.
226.	谷村綾子, 鎌田歩規代, 竹谷豊, 斎藤亮彦, 堀江大輔, 山本浩範, 宮本賢一, 武田英二 : 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, 2010年5月.
227.	竹谷豊, 首藤恵泉, 宮本賢一, 武田英二 : 生活習慣病の病態における栄養素トランスポーターの役割, 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, 2010年5月.
228.	谷村綾子, 鎌田歩規代, 竹谷豊, 斎藤亮彦, 堀江大輔, 山本浩範, 宮本賢一, 武田英二 : 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, 2010年5月.
229.	中橋乙起, 山本浩範, 田中更紗, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年5月.
230.	池田翔子, 山本浩範, 増田真志, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 : 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, 2010年5月.
231.	塩田あすか, 竹谷豊, 田中輝実, 佐田政隆, 山本浩範, 武田英二 : リンの過剰摂取は高脂血症モデルマウスのアテローム病変形成を減少させる, 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, 2010年5月.
232.	池田翔子, 山本浩範, 増田真志, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 : 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, 2010年5月.
233.	竹谷豊 : 各種栄養素が血管内皮に与える影響, ランチョンセミナー・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, 2010年5月.
234.	首藤恵泉, 竹谷豊, 大屋美穂, 小河真理子, 中西美咲, 阿望幾久子, 保坂利男, 山本浩範, 酒井徹, 武田英二 : 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, 2010年5月.
235.	上番増喬, 竹谷豊, 山本浩範, 阿望幾久子, 新井英一, 竹井悠一郎, 増田真志, 谷村綾子, 原田永勝, 奥村仙示, 武田英二 : 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, 2010年1月.
236.	山本浩範, 菊地浩子, 桑原頌治, 田中更沙, 中橋乙起, 竹谷豊, 宮本賢一, 佐々木一, 武田英二 : 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, 2010年1月.
237.	首藤恵泉, 竹谷豊, 阿望幾久子, 保坂利男, 山本浩範, 酒井徹, 武田英二 : 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, 2010年1月.
238.	首藤恵泉, 竹谷豊, 山本浩範, 酒井徹, 武田英二 : 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, 2009年5月.
239.	首藤恵泉, 竹谷豊, 田中理恵子, 一色政志, 阿望幾久子, 奥村仙示, 山本浩範, 武田英二 : 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, 2009年1月.
240.	首藤恵泉, 竹谷豊, 一色政志, 山本浩範, 武田英二 : 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, 2008年10月.
241.	首藤恵泉, 竹谷豊, 山本浩範, 奥村仙示, 酒井徹, 武田英二 : 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, 2008年9月.
242.	岩田武男, 水澤典子, 竹谷豊, 板倉光夫, 吉本勝彦 : 副甲状腺癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第32回日本比較内分泌学会大会, 2007年10月.
243.	岩田武男, 水澤典子, 竹谷豊, 板倉光夫, 吉本勝彦 : 癌抑制因子パラフィブロミンはSV40 large T抗原存在下では細胞増殖促進に働く, 第10回日本内分泌病理学会学術総会, 2006年11月.
244.	水澤典子, 原田永勝, 岩田武男, 国香清, 森谷眞紀, 竹谷豊, 板倉光夫, 吉本勝彦 : 膵β細胞に高発現する新規蛋白Isletasinの機能解析, 第49回日本糖尿病学会年次学術集会, 2006年5月.
245.	岩田武男, 水澤典子, 竹谷豊, 板倉光夫, 吉本勝彦 : 副甲状腺癌抑制遺伝子産物パラフィブロミンとSV40 large T抗原の相互作用による癌化機構, 第79回日本内分泌学会学術総会, 2006年5月.
246.	竹谷豊 : 糖尿病にならないための栄養の知識, 那加川町健康福祉課講演, 2005年12月.
247.	西田由香, 奥村仙示, 竹谷豊, 山本浩範, 武田英二 : 急性高リン負荷によるFGF23の応答, 中外製薬株式会社講演, 2005年12月.
248.	西田由香, 奥村仙示, 竹谷豊, 山本浩範, 武田英二 : 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, 2005年12月.
249.	澤田直樹, 竹谷豊, 梨木邦剛, 山本浩範, 新井英一, 武田英二 : 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, 2005年12月.
250.	竹谷豊, 中村麻子, 梨木邦剛, 谷村綾子, 山本浩範, 宮本賢一, 武田英二 : 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, 2005年12月.
251.	西田由香, 奥村仙示, 竹谷豊, 山本浩範, 武田英二 : 高リン負荷に対するFGF23の応答, 徳島骨代謝研究会, Vol.12, 2005年10月.
252.	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.
253.	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.
254.	奥村仙示, 谷口章子, 西田由香, 竹内晴美, 首藤惠泉, 新井英一, 竹谷豊, 武田英二 : 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, 2005年9月.
255.	首藤惠泉, 竹谷豊, 西田由香, 奥村仙示, 新井英一, 武田英二 : 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, 2005年9月.
256.	竹谷豊 : リン酸トランスポーターの調節におけるezrinの役割, 瀬戸内カンファレンス, Vol.9, 2005年8月.
257.	岩田武男, 水澤典子, 竹谷豊, 板倉光夫, 吉本勝彦 : Under40 Panel Discussion 副甲状腺癌抑制遺伝子産物パラフィブロミンと相互作用する蛋白の同定, 第78回日本内分泌学会学術総会, 2005年7月.
258.	辻光義, 山本浩範, 佐藤匡俊, 竹谷豊, 加藤茂明, 稲熊隆博, 武田英二 : 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, 2005年7月.
259.	西田由香, 奥村仙示, 竹谷豊, 佐藤匡俊, 山本浩範, 武田英二 : 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, 2005年7月.
260.	竹谷豊, 梨木邦剛, 山本浩範, 佐藤匡俊, 武田英二 : 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, 2005年7月.
261.	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.
262.	辻光義, 山本浩範, 佐藤匡俊, 竹谷豊, 庄子佳文子, 稲熊隆博, 武田英二 : 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, 2005年5月.
263.	武藤佳瑞智, 新井英一, 水野昭, 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, 竹谷豊, 山本浩範, 土井俊夫, 武田英二 : 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, 2005年5月.
264.	竹井悠一郎, 山本浩範, 梨木邦剛, 竹谷豊, 武田英二 : 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, 2005年5月.
265.	石黒真理子, 山本浩範, 竹井悠一郎, 竹谷豊, 武田英二 : 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, 2005年5月.
266.	辻光義, 山本浩範, 佐藤匡俊, 竹谷豊, 庄子佳文子, 稲熊隆博, 武田英二 : 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, 2005年5月.
267.	深谷牧子, 新井英一, 水野昭, 松尾薫, 奥村仙示, 山本浩範, 竹谷豊, 武田英二 : 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, 2005年5月.
268.	谷口章子, 奥村仙示, 西田由香, 竹内晴美, 新井英一, 山本浩範, 竹谷豊, 武田英二 : 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, 2005年5月.
269.	梨木邦剛, 首藤惠泉, 西田由香, 奥村仙示, 新井英一, 山本浩範, 竹谷豊, 武田英二 : 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, 2005年5月.
270.	谷口章子, 奥村仙示, 西田由香, 竹内晴美, 新井英一, 山本浩範, 竹谷豊, 武田英二 : 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, 2005年5月.
271.	新井英一, 佐久間理英, 須浪聖香, 松尾薫, 深谷牧子, 武藤佳瑞智, 水野昭, 佐々木一, 有馬裕史, 水本憲司, 奥村仙示, 竹谷豊, 武田英二 : 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, 2005年2月.
272.	竹谷豊 : 骨粗鬆症を予防するための食生活, 羽ノ浦町健康福祉課講演, 2005年1月.
273.	松尾薫, 新井英一, 武藤佳瑞智, 深谷牧子, 佐久間理英, 水野昭, 水本憲司, 麻生高伸, 有馬裕史, 佐々木一, 竹谷豊, 土井俊夫, 武田英二 : 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, 2005年1月.
274.	山本浩範, 木村宏子, 辻光義, 石黒真理子, 竹井悠一郎, 佐藤匡俊, 宮本賢一, 白神俊幸, 田中裕子, 新井英一, 竹谷豊, 武田英二 : 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, 2005年1月.
275.	竹谷豊 : 寝たきり予防の栄養学, 井川町健康大学講演, 2004年12月.
276.	庄野朱美, 塚口裕康, 矢尾板永信, 行田正晃, 竹谷豊, 山本格, 土井俊夫 : ポドサイト細胞接着装置における脂質マクロドメインの多様性-糸球体硬化症遺伝子産物Podocinと接着因子Coxsackievirus and Adenovirus receptor(CAR)を用いた解析, 日本分子生物学会年会, Vol.27, 2004年12月.
277.	竹谷豊 : 骨粗鬆症の病態と栄養管理, 岐阜県栄養士会岐阜支部会講演, 2004年10月.
278.	竹谷豊 : 骨代謝の基礎と骨粗鬆症の病態，栄養療法, 2004年度第4回CNP研究会講演, 2004年10月.
279.	奥村仙示, 竹内晴美, 西田由香, 谷口章子, 新井英一, 竹谷豊, 武田英二 : 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, 2004年10月.
280.	武田英二, 竹内里美, 竹内晴美, 奥村仙示, 新井英一, 竹谷豊, 山田静恵, 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, 2004年10月.
281.	佐久間理英, 新井英一, 須波聖香, 松尾薫, 深谷牧子, 武藤佳瑞智, 水野昭, 佐々木一, 有馬裕史, 水本憲司, 奥村仙示, 山本浩範, 竹谷豊, 武田英二 : 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, 2004年10月.
282.	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.
283.	竹谷豊 : 病気になっても寝込まない栄養学, 阿南市保健センター講演, 2004年9月.
284.	武田英二, 竹谷豊, 山本浩範 : 「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, 2004年8月.
285.	山本浩範, 佐藤匡俊, 庄子佳文子, 梨木邦剛, 竹谷豊, 稲熊隆博, 武田英二 : 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, 2004年8月.
286.	佐藤匡俊, 山本浩範, 竹谷豊, 武田英二 : 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, 2004年8月.
287.	山本浩範, 梨木邦剛, 竹谷豊, 佐藤匡俊, 武田英二 : 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, 2004年8月.
288.	竹谷豊, 梨木邦剛, 武市朋子, 山本浩範, 武田英二 : 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, 2004年8月.
289.	武田英二, 竹谷豊, 新井英一 : 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, 2004年6月.
290.	辻光義, 山本浩範, 三木田愛, 佐藤匡俊, 庄子佳文子, 新井英一, 竹谷豊, 稲熊隆博, 武田英二 : 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, 2004年5月.
291.	佐藤匡俊, 山本かおり, 山本浩範, 新井英一, 竹谷豊, 武田英二 : 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, 2004年5月.
292.	竹内晴美, 竹内里美, 奥村仙示, 中村多希, 新井英一, 竹谷豊, 三宅秀則, 田代征記, 武田英二 : 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, 2004年5月.
293.	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.
294.	梨木邦剛, 武市朋子, 竹谷豊, 武田英二 : 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, 2004年5月.
295.	山本浩範, 三木田愛, 辻光義, 佐藤匡俊, 山本かおり, 庄子佳文子, 新井英一, 竹谷豊, 稲熊隆博, 武田英二 : 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, 2004年5月.
296.	新井英一, 水野昭, 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, 山本浩範, 竹谷豊, 武田英二 : 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, 2004年5月.
297.	新井英一, 水野昭, 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, 竹谷豊, 土井俊夫, 武田英二 : 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, 2004年5月.
298.	新井英一, 水野昭, 竹谷豊, 佐々木一, 有馬裕史, 松浦基, 水本憲司, 一色宏之, 土井俊夫, 武田英二 : 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, 2004年1月.
299.	深谷牧子, 佐久間理英, 新井英一, 水野昭, 松尾薫, 武藤佳瑞智, 佐々木一, 有馬裕史, 松浦基, 水元憲司, 竹谷豊, 土井俊夫, 武田英二 : 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, 2004年1月.
300.	M. Ichikawa, 竹谷豊, K. Kobayashi, K. Nashiki, N. Sawada, 武田英二 : ESTABLISHMENT OF THE ELISA SYSTEM FOR CAVEOLIN-1, 日本生化学会大会, Vol.76, 2003年10月.
301.	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.
302.	竹谷豊, 新井英一, 奥村仙示, 武田英二 : 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, 2003年9月.
303.	武田英二, 奥村仙示, 新井英一, 竹谷豊 : 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, 2003年9月.
304.	山本浩範, 竹谷豊 : フラボノイドによるカルシウム骨代謝調節, 瀬戸内カンファレンス, Vol.7, 2003年8月.
305.	武田英二, 新井英一, 水野昭, 松尾薫, 深谷牧子, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 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, 2003年7月.
306.	Yutaka Taketani : Subcellular localization and translocational regulation of type II asodium-dependent phosphate transporter (NaPi-IIa) by PTH In renal proximal tubular cells, 小児代謝性骨疾患研究大阪国際会議場, Vol.20, Jun. 2003.
307.	佐藤匡俊, 森田恭子, 加堂有紀, 竹谷豊, 新居佳孝, 武田英二 : 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, 2003年5月.
308.	新井英一, 水野昭, 松尾薫, 深谷牧子, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 土井俊夫, 武田英二 : 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, 2003年5月.
309.	佐藤匡俊, 森田恭子, 加堂有紀, 竹谷豊, 新居佳孝, 武田英二 : 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, 2003年5月.
310.	新井英一, 松尾薫, 深谷牧子, 水野昭, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 土井俊夫, 武田英二 : 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, 2003年5月.
311.	武田英二, 新井英一, 庄司有里, 粟根尚美, 水野昭, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 土井俊夫 : 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, 2003年5月.
312.	竹谷豊, 網塚憲生, 小川千春, 澤田直樹, 野本香, 武田英二 : 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, 2003年5月.
313.	新井英一, 庄司有里, 粟根尚美, 深谷牧子, 松尾薫, 竹谷豊, 武田英二, 水野昭, 土井俊夫, 佐々木一, 有馬裕史, 松浦基, 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, 2003年5月.
314.	武田英二, 水野昭, 新井英一, 庄司有里, 粟根尚美, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 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, 2003年1月.
315.	新井英一, 水野昭, 庄司有里, 粟根尚美, 佐々木一, 有馬裕史, 松浦基, 竹谷豊, 土井俊夫, 武田英二 : 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, 2003年1月.
316.	梨木邦剛, 竹谷豊, 森田恭子, 武田英二 : 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, 2002年11月.
317.	竹谷豊, 奥村仙示, 森田恭子, 新井英一, 武田英二 : 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, 2002年11月.
318.	武田英二, 新井英一, 竹谷豊, 森田恭子, 奥村仙示 : 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, 2002年11月.
319.	中村多希, 奥村仙示, 津田紀子, 新井英一, 竹谷豊, 三宅秀則, 田代征記, 水野昭, 土井俊夫, 武田英二 : 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, 2002年11月.
320.	竹谷豊, 梨木邦剛, 澤田直樹, 森田恭子, 武田英二 : 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, 2002年10月.
321.	竹谷豊, 野本真由美, 山本浩範, 一色政志, 加藤茂明, 武田英二 : 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, 2002年7月.
322.	梨木邦剛, 竹谷豊, 森田恭子, 武田英二 : 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, 2002年7月.
323.	佐藤匡俊, 森田恭子, 大久保公美, 竹谷豊, 新居佳孝, 武田英二 : 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, 2002年7月.
324.	竹谷豊 : 食品学・食品加工学, 株式会社西洋フードシステムズ講義, 2002年4月.
325.	野本真由美, 竹谷豊, 山本浩範, 一色政志, 加藤茂明, 武田英二 : 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, 2002年4月.
326.	山本浩範, 小林くみ, 竹谷豊, 森田恭子, 新井英一, 武田英二, 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, 2001年8月.
327.	小林くみ, 山本浩範, 谷佳子, 竹谷豊, 森田恭子, 新井英一, 宮本賢一, 武田英二 : 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, 2001年5月.
328.	宮本賢一, 新居智子, 瀬川博子, 伊藤美紀子, 竹谷豊, 武田英二, 金井好克, 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, 2001年5月.

その他・研究会:

1.	竹谷豊 : 慢性腎臓病とたんぱく質栄養，第1回食肉と健康を考えるフォーラム委員会, 2021年8月.
2.	吉澤和香, 中尾真理, 伊美友紀子, 矢引紀江, 新井田裕樹, 増田真志, 奥村仙示, 竹谷豊 : 慢性腎臓病に伴う骨ミネラル代謝異常(CKD-MBD)における骨ー筋連関, 第3回日本CKD-MBD研究会学術集会(御茶ノ水ソラシティカンファレンスセンター), 2019年3月.
3.	林眞由, 福田詩織, 岸本麻希, 増田真志, 奥村仙示, 山本浩範, 竹谷豊 : 妊娠前における食餌性リン負荷が仔のリン・ビタミンD代謝調節系に及ぼす影響, 第3回日本CKD-MBD研究会学術集会(御茶ノ水ソラシティカンファレンスセンター), 2019年3月.
4.	増田真志, 山本浩範, Yimamu Yilimulati, 大谷彩子, 大西里奈, 武田英二, 竹谷豊 : 第2回 Neo Vitamin D Workshop 学術集会, 2016年8月.
5.	竹谷豊 : 慢性腎臓病におけるリンとビタミンD, 脂溶性ビタミン総合研究委員会，松島一ノ坊，宮城県松島町，2015年12月4日, 2015年12月.
6.	奥村仙示, 竹谷豊, 武田英二 : 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, 第14回日本先進糖尿病治療研究会, 2014年12月.
7.	竹谷豊 : リン代謝異常と血管機能障害, 第27回ROD-21研究会，名古屋市，2013年2月9日, 2013年2月.
8.	武田英二, 山本浩範, 大谷彩子, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 冨永辰也, 土井俊夫 : 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, 2012年3月.
9.	竹谷豊 : 腎不全モデルラットにおけるリン制限食による血管内皮機能障害改善効果, 第30回腎と骨代謝研究会学術集会, 2011年10月.
10.	山本浩範, 大谷彩子, 横山望, 香西美奈, 竹谷豊, 武田英二 : 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, 2011年7月.
11.	増田真志, 山本浩範, 香西美奈, 竹井悠一郎, 中橋乙起, 池田翔子, 大谷彩子, 竹谷豊, 宮本賢一, 武田英二 : 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, 2011年1月.
12.	中橋乙起, 山本浩範, 田中更沙, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 : 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, 2010年11月.
13.	橋本脩平, 山本浩範, 竹谷豊, 武田英二 : 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, 2010年11月.
14.	竹谷豊 : 栄養学的に見た高リン血症の問題, 第13回東海ROD研究会，名古屋，平成22年7月31日, 2010年7月.
15.	山本浩範, 菊地浩子, 田中更沙, 中橋乙起, 中尾真理, 竹谷豊, 安西尚彦, 武田英二 : 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, 2010年7月.
16.	竹谷豊 : 栄養学教室における内皮機能検査, 血管不全研究会第8回学術集会，東京，平成22年4月10日, 2010年4月.
17.	竹谷豊, 山本浩範 : リン酸トランスポーターの調節におけるezrinの役割, 第9回瀬戸内カンファレンス, 2005年8月.
18.	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.
19.	梨木邦剛, 武市朋子, 竹谷豊, 武田英二 : 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, 2004年8月.
20.	佐藤匡俊, 山本浩範, 竹谷豊, 武田英二 : 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, 2004年7月.
21.	竹谷豊, 梨木邦剛, 武市朋子, 武田英二 : 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, 2003年12月.
22.	武田英二, 野本真由美, 山本浩範, 竹谷豊, 一色政志, 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, 2002年9月.
23.	竹谷豊, 武田英二, 森田恭子 : 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, 2002年6月.
24.	野本真由美, 竹谷豊, 山本浩範, 武田英二 : 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, 2001年12月.
25.	野本真由美, 山本浩範, 竹谷豊, 森田恭子, 武田英二 : 無機リン酸による1α水酸化酵素の発現調節, 徳島Bone Forum, 2001年12月.

報告書:

1.	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. (要約) 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. (キーワード) Animals / Antioxidants / Aorta, Thoracic / Cattle / Cell Culture Techniques / Cells, Cultured / Dose-Response Relationship, Drug / Endothelium, Vascular / Fluorescent Dyes / グルコース (glucose) / Hyperglycemia / Microscopy, Confocal / 一酸化窒素 (nitric oxide) / 酸化ストレス (oxidative stress) / 活性酸素 (reactive oxygen species) / Time Factors (徳島大学機関リポジトリ) ● Metadata: 111585 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.52.295 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16366519 ● Summary page in Scopus @ Elsevier: 2-s2.0-30144439691 (徳島大学機関リポジトリ: 111585, DOI: 10.2152/jmi.52.295, PubMed: 16366519, Elsevier: Scopus)
2.	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. (要約) 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. (キーワード) 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 (徳島大学機関リポジトリ) ● Metadata: 111562 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.52.259 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111562, DOI: 10.2152/jmi.52.259, PubMed: 16366512)

特許:

1.	羽田尚彦, 井上淳詞, 豊田太, 竹谷豊 : 食品，悪心，嘔吐抑制剤及び医薬部外品, 特願2016-036817, 特開2017-154979, 特許第6583787号 (2019年9月).
2.	竹谷豊, 武田英二 : 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, 特願2005319349 (2005年11月), 特開2007126383 (2007年5月), 特許第4839436号 (2011年10月).

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

プレシジョン栄養学の実現を目指した経世代エピゲノム栄養学の研究基盤の確立 (研究課題/領域番号: 23K28019 )
運動による血清リン調節作用の解明とCKD-MBDの予防・治療への応用 (研究課題/領域番号: 19K22811 )
体内リンセットポイントの分子機序解明と老化関連病変の新たな治療標的への応用 (研究課題/領域番号: 19H04053 )
慢性腎臓病における脂質代謝異常による筋萎縮発生機序の解明 (研究課題/領域番号: 17K19910 )
エピゲノム変化を指標とした新しい食事評価研究手法（エピゲノム食事学）の確立 (研究課題/領域番号: 16H03046 )
食事性リンの感知機構の解明と副甲状腺ホルモン初期分泌障害の病態概念の確立 (研究課題/領域番号: 26560057 )
生体リンセンシング機構の統合的理解と生活習慣病予防への応用 (研究課題/領域番号: 25282022 )
慢性腎臓病の新たな栄養指導法開発を目指したリン負荷指数の理論と技術基盤の確立 (研究課題/領域番号: 24650424 )
健康から発病に至る心理的・生理的変化および栄養代謝変化の解明 (研究課題/領域番号: 24300256 )
ニュートリゲノミクス解析に基づく分子食育学の研究基盤の確立 (研究課題/領域番号: 22650181 )
栄養素代謝バランス統合制御システムの分子基盤と生活習慣病発症にお (研究課題/領域番号: 22300237 )
食生活での栄養素相互作用と臓器代謝調節ネットワーク機構の解明 (研究課題/領域番号: 21300277 )
健康長寿の基盤となる新たな栄養シグナルの発見と疾病予防における役割 (研究課題/領域番号: 19680030 )
リン代謝調節におけるリン酸トランスポーターエンドサイトーシス複合体の構造と機能 (研究課題/領域番号: 17790554 )
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 (研究課題/領域番号: 17650225 )
無機リン酸トランスポートソームの機能制御とその破綻 (研究課題/領域番号: 17081013 )
細胞外への小胞分泌機構の解明 (研究課題/領域番号: 14780548 )
リン生体調節を制御する複合的リン濃度感知システムの解明 (研究課題/領域番号: 13470013 )
新規カルシウム・リン代謝調節ホルモン(フォスファトニン)の測定法の開発 (研究課題/領域番号: 10557096 )
腎臓に存在するリン応答性転写調節因子の同定 (研究課題/領域番号: 09770845 )
無機リン酸によるナトリウム/リン酸共輸送担体遺伝子発現調節機構の解明 (研究課題/領域番号: 07770105 )
ラジオアイソトープを用いない血中1,25-ジヒドロキシビタミンD濃度測定法の開発 (研究課題/領域番号: 07557321 )
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教授 : 竹谷 豊

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教授 : 竹谷豊