Tokushima University / Educator and Researcher Directory --- Sakaue, Hiroshi

Personal Web Page

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

https://orcid.org/0000-0002-2468-2363 (ORCID)

Field of Study

○	糖尿病・肥満

Subject of Study

○	脂肪細胞の分化・増殖機構とライフサイクルの解明に関する研究, 脂肪細胞制御によるメタボリックシンドローム治療法の開発に関する研究 (diabetes, obesity, adipocyte, adipocytekine, cell proliferation and differentiation, transcription factor)

Book / Paper

Book:

1.	Hiroshi Sakaue : 血管内皮機能改善作用を有する新たな機能性脂質の同定, 日本水産油脂協会, Jun. 2023. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1130296486348585998 (CiNii: 1130296486348585998)
2.	Yutaka Taketani, 塚原丘美, 桑波田雅士 and Hiroshi Sakaue : 新・臨床栄養学第2版, Kodansha, Tokyo, Mar. 2023. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1130014316335459844 (CiNii: 1130014316335459844)
3.	Masashi Masuda, Hironori Yamamoto, 竹井悠一郎, 中橋乙起, 足立雄一郎, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Hiroshi Sakaue, 宮崎淳, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b), The Vitamin Society of Japan, Nov. 2020. (Summary) ビタミン欠乏(VAD)ラットにall-transレチノイン酸(ATRA)を投与後，腸管のNpt2b発現を中心としたリン吸収への影響と，ラットNpt2b遺伝子プロモーターを用いたATRAによるNpt2b生化学転写調節機構について検討した．VADラットにATRAを腹腔内投与した18時間後，血漿リン濃度はビタミンAによる影響を認めなかったが，腸管リン酸取り込み活性，Npt2b蛋白発現量およびmRNA発現量はATRA投与により抑制された．マウス胎児線維芽細胞株NIH3T3細胞を用いたルシフェラーゼアッセイの結果，レチノイン酸受容体(RAR)/レチノイドX受容体存在下においてATRAおよびRARアゴニスト濃度依存的にNpt2b遺伝子プロモーター活性は低下した．デリーションアッセイの結果，ATRAによるNpt2b遺伝子プロモーター活性の低下は，転写因子CCAAT/enhancer-binding protein(C/EBP)依存的であることが示唆された． (Keyword) all-trans retinoic acid (ATRA) / retinoic acid receptor (RAR) / CCAAT/enhancer-binding protein (C/EBP) / small intestine / type II sodium-dependent phosphate co-transporter (Npt2b) (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.94.11_545 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390571704642711680 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.94.11_545 (DOI: 10.20632/vso.94.11_545, CiNii: 1390571704642711680)
4.	Eiji Takeda, Yoshiko Suzuki, Akiko Matsumura, Yutaka Nakaya, Rie Tsutsumi, Hiroshi Sakaue, Yasuhiro Hamada, Akiko Hata and 他42人 : Guidebook of Nutrition Support Team 2017, 5th Edition, Jul. 2017.
5.	竹谷豊, 塚原丘美, 桑波田雅士 and Hiroshi Sakaue : 新・臨床栄養学 (栄養科学シリーズNEXT) 改訂, Kodansha, Jan. 2016.
6.	Rie Tsutsumi, Hiroshi Sakaue and Yasuo Tsutsumi : Aug. 2015.
7.	Hiroshi Sakaue : 徳島大学附属図書館私のこの一冊, 徳島大学附属図書館, Tokushima, Apr. 2014.
8.	Hidekazu Arai, Hiroshi Sakaue, Eiji Takeda, Yutaka Taketani, 藤岡由夫 and 細川雅也 : 臨床病態栄養学第3版, 文光堂, Sep. 2013.
9.	Hiroshi Sakaue : 糖尿病イラストレイテッド, 羊土社, Mar. 2012.
10.	岡田裕子, Hiroshi Sakaue and 春日雅人 : 肥満症のくすり, 日本評論社, Apr. 2011.
11.	Hiroshi Sakaue : がん栄養ハンドブック, Medical Review Co.,Ltd, Osaka, Jan. 2011.
12.	Hiroshi Sakaue : NSTガイドブック2011 リフィーディング症候群の予防と治療, メディカルレビュー社, Jan. 2011.
13.	Hiroshi Sakaue : 糖尿病ナビゲーター脂肪細胞分化, メディカルレビュー社, Sep. 2010.

Academic Paper (Judged Full Paper):

1.	Ayuka Kawakami, Mika Bandou, Tomoe Takashi, Mizuki Sugiuchi, Mizusa Hyodo, Yuna Mishima, Masashi Kuroda, Hiroyasu Mori, Akio Kuroda, Hiromichi Yumoto, Munehide Matsuhisa, Hiroshi Sakaue and Rie Tsutsumi : Umami taste sensitivity is associated with food intake and oral environment in subjects with diabetes, The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 241-250, 2023. (Summary) Dysgeusia is a serious problem in patients with diabetes because it often leads to overeating, which is associated with disease progression. This study aimed to investigate the association between taste sensitivity, eating habits, and the oral environment. In this cross-sectional study of 75 subjects with diabetes, gustatory function was assessed using the whole-mouth method, and lingual taste receptor gene expression was measured by real-time PCR. Food intake was evaluated using a food frequency questionnaire based on food groups. The oral environment was assessed using xerostomia and periodontal comprehensive examination. In total, 45.3%, 28.0%, and 18.7% of subjects showed lower umami taste sensitivity, low sweet taste sensitivity, and low salt taste sensitivity, respectively. Lower umami sensitivity correlated with lower estimated glomerular filtration rate and higher energy-source food intake. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression than those with lower plaque control record. Reduced umami taste sensitivity is associated with decreased renal function and high energy food intake in diabetes. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression, suggesting that the oral environment affects taste gene expression. J. Med. Invest. 70 : 241-250, February, 2023. (Keyword) Humans / Taste / Cross-Sectional Studies / Taste Perception / Diabetes Mellitus / Eating (Tokushima University Institutional Repository) ● Metadata: 118208 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164729 ● Summary page in Scopus @ Elsevier: 2-s2.0-85158866092 (Tokushima University Institutional Repository: 118208, DOI: 10.2152/jmi.70.241, PubMed: 37164729, Elsevier: Scopus)
2.	Bingzi Dong, Masahiro Hiasa, Yoshiki Higa, Yukiyo Ohnishi, Itsuro Endo, Takeshi Kondo, Yuichi Takashi, Maria Tsoumpra, Risa Kainuma, Shun Sawatsubashi, Hiroshi Kiyonari, Go Shioi, Hiroshi Sakaue, Tomoki Nakashima, Shigeaki Kato, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : Osteoblast/osteocyte-derived interleukin-11 regulates osteogenesis and systemic adipogenesis., Nature Communications, Vol.13, No.1, 2022. (Summary) did not exhibit any abnormalities. We demonstrate that osteoblast/osteocyte-derived IL-11 controls both osteogenesis and systemic adiposity in response to mechanical loading, an important insight for our understanding of osteoporosis and metabolic syndromes. (Keyword) Animals / Mice / Adipogenesis / Interleukin-11 / Obesity / Osteoblasts / Osteocytes / Osteogenesis / Mice, Knockout (Tokushima University Institutional Repository) ● Metadata: 118940 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41467-022-34869-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36424386 ● Search Scopus @ Elsevier (PMID): 36424386 ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-022-34869-3 (Tokushima University Institutional Repository: 118940, DOI: 10.1038/s41467-022-34869-3, PubMed: 36424386)
3.	Masato Tagi, Mari Tajiri, Yasuhiro Hamada, Yoshifumi Wakata, Xiao Shan, Kazumi Ozaki, Masanori Kubota, Sosuke Amano, Hiroshi Sakaue, Yoshiko Suzuki and Jun Hirose : Accuracy of an Artificial Intelligence-Based Model for Estimating Leftover Liquid Food in Hospitals: Validation Study., JMIR Formative Research, Vol.6, No.5, e35991, 2022. (Summary) An accurate evaluation of the nutritional status of malnourished hospitalized patients at a higher risk of complications, such as frailty or disability, is crucial. Visual methods of estimating food intake are popular for evaluating the nutritional status in clinical environments. However, from the perspective of accurate measurement, such methods are unreliable. The accuracy of estimating leftover liquid food in hospitals using an artificial intelligence (AI)-based model was compared to that of visual estimation. The accuracy of the AI-based model (AI estimation) was compared to that of the visual estimation method for thin rice gruel as staple food and fermented milk and peach juice as side dishes. A total of 576 images of liquid food (432 images of thin rice gruel, 72 of fermented milk, and 72 of peach juice) were used. The mean absolute error, root mean squared error, and coefficient of determination (R) were used as metrics for determining the accuracy of the evaluation process. Welch t test and the confusion matrix were used to examine the difference of mean absolute error between AI and visual estimation. The mean absolute errors obtained through the AI estimation approach were 0.63 for fermented milk, 0.25 for peach juice, and 0.85 for the total. These were significantly smaller than those obtained using the visual estimation approach, which were 1.40 (P<.001) for fermented milk, 0.90 (P<.001) for peach juice, and 1.03 (P=.009) for the total. By contrast, the mean absolute error for thin rice gruel obtained using the AI estimation method (0.99) did not differ significantly from that obtained using visual estimation (0.99). The confusion matrix for thin rice gruel showed variation in the distribution of errors, indicating that the errors in the AI estimation were biased toward the case of many leftovers. The mean squared error for all liquid foods tended to be smaller for the AI estimation than for the visual estimation. Additionally, the coefficient of determination (R) for fermented milk and peach juice tended to be larger for the AI estimation than for the visual estimation, and the R value for the total was equal in terms of accuracy between the AI and visual estimations. The AI estimation approach achieved a smaller mean absolute error and root mean squared error and a larger coefficient of determination (R) than the visual estimation approach for the side dishes. Additionally, the AI estimation approach achieved a smaller mean absolute error and root mean squared error compared to the visual estimation method, and the coefficient of determination (R) was similar to that of the visual estimation method for the total. AI estimation measures liquid food intake in hospitals more precisely than visual estimation, but its accuracy in estimating staple food leftovers requires improvement. (Tokushima University Institutional Repository) ● Metadata: 117555 (Link to Publication Site) ● Publication site (DOI): 10.2196/35991 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35536638 ● Search Scopus @ Elsevier (PMID): 35536638 ● Search Scopus @ Elsevier (DOI): 10.2196/35991 (Tokushima University Institutional Repository: 117555, DOI: 10.2196/35991, PubMed: 35536638)
4.	Hiroshi Sakaue, Masashi Kuroda and Rie Tsutsumi : 徳島県民が知っておくべき予防医学∼病気にならないための秘訣∼ 肥満から読み解く高齢者の栄養の問題点と管理, Shikoku Acta Medica, Vol.78, No.1-2, 3-8, 2022. (Summary) The shift of Japanese eating habits from salty and grain-based consumption with low animal protein to a diet with a variety of lipids and animal products after Second World War has significantly reduced the rate of infections and cerebral bleeding. On the other hand, the increase in life-style related diseases such as cancer, heart disease, stroke, diabetes has become a serious problem in our country. However, it is difficult to discuss the nutrition of the elderly in a stereotype because of the diversity in physical and psychological feature. Although there are many important issues that require discussions encompassing broad aspects in taking high protein diet as a main topic, it may be possible to consider a question in the aspects of body weight or body composition in the elderly. In this section, we discuss the `secret key' in nutrition to health for the aged. (Keyword) The elderly / obesity / lifestyle-related disease / nutrition / High protein diet (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050010997647006592 (CiNii: 1050010997647006592)
5.	Kana Beppu, Rie Tsutsumi, Satoshi Ansai, Nana Ochiai, Mai Terakawa, Marie Mori, Masashi Kuroda, Kazuki Horikawa, Takumi Tomoi, Joe Sakamoto, Yasuhiro Kamei, Kiyoshi Naruse and Hiroshi Sakaue : Development of a screening system for agents that modulate taste receptor expression with the CRISPR-Cas9 system in medaka., Biochemical and Biophysical Research Communications, Vol.601, 65-72, 2022. (Summary) Taste recognition mediated by taste receptors is critical for the survival of animals in nature and is an important determinant of nutritional status and quality of life in humans. However, many factors including aging, diabetes, zinc deficiency, infection with influenza or cold viruses, and chemotherapy can trigger dysgeusia, for which a standard treatment has not been established. We here established an engineered strain of medaka (Oryzias latipes) that expresses green fluorescent protein (GFP) from the endogenous taste 1 receptor 3 (T1R3) gene locus with the use of the CRISPR-Cas9 system. This T1R3-GFP knock-in (KI) strain allows direct visualization of expression from this locus by monitoring of GFP fluorescence. The pattern of GFP expression in the T1R3-GFP KI fish thus mimicked that of endogenous T1R3 gene expression. Furthermore, exposure of T1R3-GFP KI medaka to water containing monosodium glutamate or the anticancer agent 5-fluorouracil resulted in an increase or decrease, respectively, in GFP fluorescence intensity, effects that also recapitulated those on T1R3 mRNA abundance. Finally, screening for agents that affect GFP fluorescence intensity in T1R3-GFP KI medaka identified tryptophan as an amino acid that increases T1R3 gene expression. The establishment of this screening system for taste receptor expression in medaka provides a new tool for the development of potential therapeutic agents for dysgeusia. (Keyword) Animals / CRISPR-Cas Systems / Dysgeusia / gene expression / Green Fluorescent Proteins / Oryzias / quality of life / Taste (Tokushima University Institutional Repository) ● Metadata: 116998 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2022.02.082 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35228123 ● Search Scopus @ Elsevier (PMID): 35228123 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2022.02.082 (Tokushima University Institutional Repository: 116998, DOI: 10.1016/j.bbrc.2022.02.082, PubMed: 35228123)
6.	Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression., Clinical & translational immunology, Vol.11, No.1, 2022. (Summary) TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA. (Tokushima University Institutional Repository) ● Metadata: 117260 (Link to Publication Site) ● Publication site (DOI): 10.1002/cti2.1371 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379 ● Search Scopus @ Elsevier (PMID): 35079379 ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371 (Tokushima University Institutional Repository: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379)
7.	Yuya Ikezumi, Yasushi Matsuura, Teruhiro Morishita, Noriko Ide, Isao Kitada, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue, Yutaka Taketani, Koichi Sairyo and Eiji Takeda : Necessity of daily 1000-IU vitamin D supplementation for maintaining a sufficient vitamin D status., The Journal of Medical Investigation : JMI, Vol.69, No.1.2, 135-140, 2022. (Summary) The changes in the serum 25-hydroxyvitamin D (25(OH)D) concentrations after daily 1000-IU vitamin D intake for 3 months (3-month-VD), 6 months (6-month-VD) and then 6-month cessation of vitamin D in-take (6-month-VD cessation) were examined. The serum 25(OH)D levels in 11 male and 16 female subjects were 12.1±3.5 ng/mL at baseline, increased to 27.1±4.7 ng/mL at 3-month-VD, 28.5±5.1 ng/mL at 6-month-VD and decreased to 16.4±4.0 ng/mL at 6-month-VD cessation. The present study suggested that a vitamin D intake of 1000 IU/day is required to maintain the 25(OH) D concentration at 30 ng/mL or higher without vitamin D intoxication. J. Med. Invest. 69 : 135-140, February, 2022. (Keyword) Dietary Supplements / female / Humans / male / Nutritional Status / vitamin D / Vitamin D Deficiency / Vitamins (Tokushima University Institutional Repository) ● Metadata: 117024 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.135 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466135 ● Search Scopus @ Elsevier (PMID): 35466135 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.135 (Tokushima University Institutional Repository: 117024, DOI: 10.2152/jmi.69.135, PubMed: 35466135)
8.	Kana Beppu, Ayuka Kawakami, Yuna Mishima, Rie Tsutsumi, Masashi Kuroda, Hiroyasu Mori, Akio Kuroda, Munehide Matsuhisa and Hiroshi Sakaue : Taste receptor gene expression is associated with decreased eGFR in patients with diabetes., The Journal of Medical Investigation : JMI, Vol.69, No.1.2, 120-126, 2022. (Summary) Dysgeusia is not only associated with zinc deficiency but also with certain drugs or diseases, including diabetes and renal failure. It often lowers the patient's quality of life and hinders access to proper nutrition. The underlying mechanism is unclear and there is a lack of awareness among patients. Here, we focused on lingual taste receptor gene expression in diabetes and elucidated the relationship between taste receptor gene expression and renal function. Forty-seven patients with diabetes and 10 healthy subjects (control group) were enrolled. Lingual foliate papillae were scraped and the derived cDNA was quantified by real-time polymerase chain reaction. Dysgeusia was assessed using SALSAVE?. All statistical analyses were performed using JMP? software 13. The expression of T1R1 and T1R2 was significantly upregulated in type 2 diabetes patients as compared with that in healthy subjects (P<0.01) but did not change in type 1 diabetes patients. T1R3 expression positively correlated and Scnn1 expression negatively correlated with estimated glomerular filtration rate, suggesting that altered taste receptor gene expression could reflect impaired renal function. Thus, alterations in T1R3 and Scnn1 expression in diabetes correlated with renal function. Taste receptor gene expression dysregulation could indicate dysgeusia associated with impaired renal function in patients with diabetes. J. Med. Invest. 69 : 120-126, February, 2022. (Keyword) Diabetes Mellitus, Type 2 / Dysgeusia / Gene Expression / Humans / Quality of Life / Receptors, G-Protein-Coupled / Taste (Tokushima University Institutional Repository) ● Metadata: 117023 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.120 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466133 ● Search Scopus @ Elsevier (PMID): 35466133 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.120 (Tokushima University Institutional Repository: 117023, DOI: 10.2152/jmi.69.120, PubMed: 35466133)
9.	Rie Tsutsumi, 三島優奈, 川上歩花, Masashi Kuroda and Hiroshi Sakaue : 生活習慣病と栄養学 : 最近のトピックスを交えて, Shikoku Acta Medica, Vol.77, No.5-6, 187-192, 2021. (Summary) Metabolic syndrome is a pathological condition with hyperglycemia, dyslipidemia, or hypertension resulting in cardiovascular and cerebrovascular disease. Factors that affect visceral fat accumulation and weight gain include not only physiological factors such as heredity, constitution, and age, but also behavioral factors and environmental factors. Eating behavior and eating environment are critical for the prevention and treatment of metabolic syndrome. In this report, we will discuss about recent topics of nutrition in metabolic syndrome, especially association with macronutrients such as carbohydrate, fatty acids and protein. In recent years, several publications have determined the benefit of low carbohydrate diet on obesity and diabetes, and the American Diabetes Association has also recommended low carbohydrate diet, Mediterranean diet, and a diet mainly consistent with vegetables and plants. There have been many reports that the effect of carbohydrate restriction has not only the weight loss effect but also reduces risk factors such as cardiovascular disease and cerebrovascular disease. Fanelli et al . recently have shown that half of US adults with diabetes have less than the recommended daily intake of protein, which may lead to poor dietary quality. Diabetic patients with low protein intake had significantly lower dietary nutrient density and 12．5% higher carbohydrate intake, whereas diabetic patients with daily protein intake meeting the recommended amount have shown that the overall quality of the diet was high and almost met the recommended daily amount of vegetables, whole grains, dairy products and added sugars. Therefore, in addition to the prevention of metabolic syndrome, protein is important for treatment of metabolic syndrome and higher QOL. Nutritional research needs further development to deal with metabolic syndrome. (Keyword) nutrition / metabolic syndrome / low carbohydrate / protein (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050292251404941184 (CiNii: 1050292251404941184)
10.	Atsushi Morio, Rie Tsutsumi, Shiho Satomi, Takashi Kondo, Hirotsugu Miyoshi, Takahiro Kato, Masashi Kuroda, Tadahiro Kitamura, Kenta Hara, Noboru Saeki, Hiroshi Sakaue and Yasuo M. Tsutsumi : Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model., Diabetology & Metabolic Syndrome, Vol.13, No.1, 2021. (Summary) Leu treatment improved the damage caused by myocardial I/R injury by promoting mTOR activity and mitochondrial fusion on prediabetic hearts in mice. (Tokushima University Institutional Repository) ● Metadata: 117442 (Link to Publication Site) ● Publication site (DOI): 10.1186/s13098-021-00755-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34801078 ● Search Scopus @ Elsevier (PMID): 34801078 ● Search Scopus @ Elsevier (DOI): 10.1186/s13098-021-00755-z (Tokushima University Institutional Repository: 117442, DOI: 10.1186/s13098-021-00755-z, PubMed: 34801078)
11.	Masato Miyake, Jun Zhang, Akihiro Yasue, Satoshi Hisanaga, Kazue Tsugawa, Hiroshi Sakaue, Miho Oyadomari, Hiroshi Kiyonari and Seiichi Oyadomari : Integrated stress response regulates GDF15 secretion from adipocytes, preferentially suppresses appetite for a high-fat diet and improves obesity., iScience, Vol.24, No.12, 2021. (Summary) The eIF2α phosphorylation-dependent integrated stress response (ISR) is a signaling pathway that maintains homeostasis in mammalian cells exposed to various stresses. Here, ISR activation in adipocytes improves obesity and diabetes by regulating appetite in a non-cell-autonomous manner. Adipocyte-specific ISR activation using transgenic mice decreases body weight and improves glucose tolerance and obesity induced by a high-fat diet (HFD) via preferential inhibition of HFD intake. The transcriptome analysis of ISR-activated adipose tissue reveals that growth differentiation factor 15 (GDF15) expression is induced by the ISR through the direct regulation of the transcription factors ATF4 and DDIT3. Deficiency in the GDF15 receptor GFRAL abolishes the adipocyte ISR-dependent preferential inhibition of HFD intake and the anti-obesity effects. Pharmacologically, 10(E), 12(Z)-octadecadienoic acid induces ISR-dependent GDF15 expression in adipocytes and decreases the intake of the HFD. Based on our findings the specific activation of the ISR in adipocytes controls the non-cell-autonomous regulation of appetite. (Tokushima University Institutional Repository) ● Metadata: 116908 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.isci.2021.103448 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34877504 ● Search Scopus @ Elsevier (PMID): 34877504 ● Search Scopus @ Elsevier (DOI): 10.1016/j.isci.2021.103448 (Tokushima University Institutional Repository: 116908, DOI: 10.1016/j.isci.2021.103448, PubMed: 34877504)
12.	Rie Tsutsumi, Yuki Yamasaki, Jiro Takeo, Hiroko Miyahara, Mayu Sebe, Masahiro Bando, Yousuke Tanba, Yuna Mishima, Kana Takeji, Nanako Ueshima, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Daiju Fukuda, Ryoko Yoshimoto, Yasuo M. Tsutsumi, Ken-ichi Aihara, Masataka Sata and Hiroshi Sakaue : Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora, Translational Research : The Journal of Laboratory and Clinical Medicine, Vol.237, 16-30, 2021. (Summary) Fish oil-derived long-chain monounsaturated fatty acids (LCMUFAs) with a carbon chain length longer than 18 units ameliorate cardiovascular risk in mice. In this study, we investigated whether LCMUFAs could improve endothelial functions in mice and humans. In a double-blind, randomized, placebo-controlled, parallel-group, multi-center study, healthy subjects were randomly assigned to either an LCMUFA oil (saury oil) or a control oil (olive and tuna oils) group. Sixty subjects were enrolled and administrated each oil for 4 weeks. For the animal study, ApoE mice were fed a Western diet supplemented with 3% of either gadoleic acid (C20:1) or cetoleic acid (C22:1) for 12 weeks. Participants from the LCMUFA group showed improvements in endothelial function and a lower trimethylamine-N-oxide level, which is a predictor of coronary artery disease. C20:1 and C22:1 oils significantly improved atherosclerotic lesions and plasma levels of several inflammatory cytokines, including IL-6 and TNF-α. These beneficial effects were consistent with an improvement in the gut microbiota environment, as evident from the decreased ratio of Firmicutes and/ or Bacteroidetes, increase in the abundance of Akkermansia, and upregulation of short-chain fatty acid (SCFA)-induced glucagon-like peptide-1 (GLP-1) expression and serum GLP-1 level. These data suggest that LCMUFAs alter the microbiota environment that stimulate the production of SCFAs, resulting in the induction of GLP-1 secretion. Fish oil-derived long-chain monounsaturated fatty acids might thus help to protect against cardiovascular disease. (Tokushima University Institutional Repository) ● Metadata: 116689 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.trsl.2021.03.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33775867 ● Summary page in Scopus @ Elsevier: 2-s2.0-85114290883 (Tokushima University Institutional Repository: 116689, DOI: 10.1016/j.trsl.2021.03.016, PubMed: 33775867, Elsevier: Scopus)
13.	Hitoshi Shono, Rie Tsutsumi, Kana Beppu, Rina Matsushima, Suzuno Watanabe, Chisa Fujimoto, Ryo Kanamura, Hiroki Ohnishi, Eiji Kondou, Takahiro Azuma, Gou Satou, Misako Kawai, Hideki Matsumoto, Yoshiaki Kitamura, Hiroshi Sakaue and Noriaki Takeda : Dietary Supplementation with Monosodium Glutamate Suppresses Chemotherapy-Induced Downregulation of the T1R3 Taste Receptor Subunit in Head and Neck Cancer Patients., Nutrients, Vol.13, No.9, 2921, 2021. (Summary) (Background) We investigated the effect of dietary supplementation with monosodium glutamate (MSG) on chemotherapy-induced downregulation of the T1R3 taste receptor subunit expression in the tongue of patients with advanced head and neck cancer. (Methods) Patients undergoing two rounds of chemoradiotherapy were randomly allocated to a control or intervention group (dietary supplementation with MSG at 2.7 g/day during the second round of chemotherapy). The relative expression of T1R3, a subunit of both umami and sweet taste receptors, in the tongue was assessed by quantitative polymerase chain reaction analysis. Dysgeusia was assessed with a visual analog scale and daily energy intake was evaluated. (Results) T1R3 expression levels in the tongue, taste sensitivity, and daily energy intake were significantly reduced after the first round of chemotherapy compared with before treatment. Furthermore, these parameters significantly decreased after the second round of chemotherapy, but the extent of decrease was significantly attenuated in the MSG group compared with the control group. (Conclusions) MSG supplementation suppresses chemotherapy-induced dysgeusia, possibly due to the inhibition of the T1R3-containing taste receptor downregulation in the tongue, thereby increasing energy intake in patients with advanced head and neck cancer. (Keyword) Adult / Aged / Aged, 80 and over / Antineoplastic Agents / Chemoradiotherapy / Dietary Supplements / Down-Regulation / Dysgeusia / Female / Head and Neck Neoplasms / Humans / Male / Middle Aged / Receptors, G-Protein-Coupled / Sodium Glutamate / Taste / Taste Buds / Tongue (Tokushima University Institutional Repository) ● Metadata: 117248 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu13092921 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34578798 ● Search Scopus @ Elsevier (PMID): 34578798 ● Search Scopus @ Elsevier (DOI): 10.3390/nu13092921 (Tokushima University Institutional Repository: 117248, DOI: 10.3390/nu13092921, PubMed: 34578798)
14.	Atsushi Morio, Rie Tsutsumi, Takashi Kondo, Hirotsugu Miyoshi, Takahiro Kato, Soshi Narasaki, Shiho Satomi, Erika Nakaya, Masashi Kuroda, Hiroshi Sakaue, Tadahiro Kitamura and Yasuo M. Tsutsumi : Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling., Nutrition, Metabolism, and Cardiovascular Diseases : NMCD, 2021. (Summary) Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.numecd.2021.06.025 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34362635 ● Search Scopus @ Elsevier (PMID): 34362635 ● Search Scopus @ Elsevier (DOI): 10.1016/j.numecd.2021.06.025 (DOI: 10.1016/j.numecd.2021.06.025, PubMed: 34362635)
15.	Manabu Ishihara, Nobuto Nakanishi, Rie Tsutsumi, Kanako Hara, Kyoka Machida, Nobuaki Yamamoto, Yasuhisa Kanematsu, Hiroshi Sakaue, Jun Oto and Yasushi Takagi : Elevated Urinary Titin and its Associated Clinical Outcomes after Acute Stroke., Journal of Stroke & Cerebrovascular Diseases, Vol.30, No.3, 2021. (Summary) Urinary titin rapidly increased after stroke and was associated with impaired functional outcomes at hospital discharge. (Keyword) Aged / Aged, 80 and over / Biomarkers / Connectin / Disability Evaluation / Female / Functional Status / Humans / Male / Middle Aged / Patient Discharge / Predictive Value of Tests / Prospective Studies / Recovery of Function / Stroke / Time Factors / Treatment Outcome / Up-Regulation / Urinalysis (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jstrokecerebrovasdis.2020.105561 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33360523 ● Search Scopus @ Elsevier (PMID): 33360523 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jstrokecerebrovasdis.2020.105561 (DOI: 10.1016/j.jstrokecerebrovasdis.2020.105561, PubMed: 33360523)
16.	Nobuto Nakanishi, Rie Tsutsumi, Kanako Hara, Masafumi Matsuo, Hiroshi Sakaue and Jun Oto : Urinary Titin N-Fragment as a Biomarker of Muscle Atrophy, Intensive Care Unit-Acquired Weakness, and Possible Application for Post-Intensive Care Syndrome., Journal of Clinical Medicine, Vol.10, No.4, 614, 2021. (Summary) Titin is a giant protein that functions as a molecular spring in sarcomeres. Titin interconnects the contraction of actin-containing thin filaments and myosin-containing thick filaments. Titin breaks down to form urinary titin N-fragments, which are measurable in urine. Urinary titin N-fragment was originally reported to be a useful biomarker in the diagnosis of muscle dystrophy. Recently, the urinary titin N-fragment has been increasingly gaining attention as a novel biomarker of muscle atrophy and intensive care unit-acquired weakness in critically ill patients, in whom titin loss is a possible pathophysiology. Furthermore, several studies have reported that the urinary titin N-fragment also reflected muscle atrophy and weakness in patients with chronic illnesses. It may be used to predict the risk of post-intensive care syndrome or to monitor patients' condition after hospital discharge for better nutritional and rehabilitation management. We provide several tips on the use of this promising biomarker in post-intensive care syndrome. (Tokushima University Institutional Repository) ● Metadata: 117559 (Link to Publication Site) ● Publication site (DOI): 10.3390/jcm10040614 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33561946 ● Search Scopus @ Elsevier (PMID): 33561946 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm10040614 (Tokushima University Institutional Repository: 117559, DOI: 10.3390/jcm10040614, PubMed: 33561946)
17.	Yasushi Matsuura, Teruhiro Morishita, Michiko Sato, Nami Sumida, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue, Yutaka Taketani, Koichi Sairyo, Akihiko Kawaura and Eiji Takeda : Effects of daily 1,000-IU vitamin D-fortified milk intake on skeletal muscle mass, power, physical function and nutrition status in Japanese., The Journal of Medical Investigation : JMI, Vol.68, No.3.4, 249-255, 2021. (Summary) An intervention study was conducted to investigate the effects of daily 1,000-IU vitamin D-fortified milk intake on skeletal muscle mass, power, physical function and nutrition status in 26 healthy people and 8 older adults living in a nursing home. The serum 25-hydroxyvitamin D [25(OH)D] level was 13.4 ± 0.8 ng / mL and it markedly increased to 29.6 ± 0.9 ng / mL after daily 1000-IU vitamin D-fortified milk intake for 6 months. Handgrip strength (kg) also significantly increased in the 21-50 years and total groups, and male subjects, and the timed up and go test signiﬁcantly improved in the 21-50 years and total groups, and female subjects after 6-month vitamin D intake. However, there were no significant differences between baseline and post-treatment in the Barthel Index (BI), walking speed (m / sec) or skeletal muscle mass (kg, % of BW, kg / m2). Therefore, the present study suggested that vitamin D-fortified milk intake is effective at improving muscle strength and physical function in Japanese, although further studies are needed, particularly for older adults. J. Med. Invest. 68 : 249-255, August, 2021. (Keyword) Aged / Animals / female / Hand Strength / Humans / Japan / male / Milk / Muscle Strength / Muscle, Skeletal / Nutritional Status / Postural Balance / Time and Motion Studies / vitamin D (Tokushima University Institutional Repository) ● Metadata: 116490 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.249 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34759139 ● Search Scopus @ Elsevier (PMID): 34759139 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.249 (Tokushima University Institutional Repository: 116490, DOI: 10.2152/jmi.68.249, PubMed: 34759139)
18.	Nobuto Nakanishi, Jun Oto, Rie Tsutsumi, Tomoko Yamamoto, Yoshitoyo Ueno, Emiko Nakataki, Taiga Itagaki, Hiroshi Sakaue and Masaji Nishimura : Effect of Electrical Muscle Stimulation on Upper and Lower Limb Muscles in Critically Ill Patients: A Two-Center Randomized Controlled Trial., Critical Care Medicine, Vol.48, No.11, e997-e1003, 2020. (Summary) In critically ill patients, electrical muscle stimulation prevented upper and lower limb muscle atrophy and attenuated proteolysis and decreased the length of hospitalization. (Keyword) Aged / Amino Acids / Critical Illness / Electric Stimulation Therapy / Extremities / Female / Humans / Male / Muscle, Skeletal / Muscular Atrophy / Quadriceps Muscle / Single-Blind Method (Tokushima University Institutional Repository) ● Metadata: 115045 (Link to Publication Site) ● Publication site (DOI): 10.1097/CCM.0000000000004522 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32897665 ● Search Scopus @ Elsevier (PMID): 32897665 ● Search Scopus @ Elsevier (DOI): 10.1097/CCM.0000000000004522 (Tokushima University Institutional Repository: 115045, DOI: 10.1097/CCM.0000000000004522, PubMed: 32897665)
19.	Yuko Okamatsu-Ogura, Masashi Kuroda, Rie Tsutsumi, Ayumi Tsubota, Masayuki Saito, Kazuhiro Kimura and Hiroshi Sakaue : UCP1-dependent and UCP1-independent metabolic changes induced by acute cold exposure in brown adipose tissue of mice., Metabolism: Clinical and Experimental, Vol.113, 154396, 2020. (Summary) These results revealed that cold exposure induces UCP1-mediated thermogenesis-dependent glucose utilization and UCP1-independent active lipid metabolism in BAT. In addition, cold exposure largely affects amino acid metabolism in BAT, especially UCP1-dependently enhances glutamine utilization. These results contribute a comprehensive understanding of UCP1-mediated thermogenesis-dependent and thermogenesis-independent metabolism in BAT. (Keyword) brown adipose tissue / Animals / Cold Temperature / fatty acids β-oxidation / Glutamine / metabolomics / knockout mice / Mice, Inbred C57BL / knockout mice / Thermogenesis / Triglycerides / Uncoupling Protein 1 (Tokushima University Institutional Repository) ● Metadata: 116598 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.metabol.2020.154396 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33065161 ● Search Scopus @ Elsevier (PMID): 33065161 ● Search Scopus @ Elsevier (DOI): 10.1016/j.metabol.2020.154396 (Tokushima University Institutional Repository: 116598, DOI: 10.1016/j.metabol.2020.154396, PubMed: 33065161)
20.	Yoko Narasaki, Michiyo Yamasaki, Sayaka Matsuura, Mayumi Morinishi, Tomomi Nakagawa, Mami Matsuno, Misaki Katsumoto, Sachi Nii, Yuka Fushitani, Kohei Sugihara, Tsuneyuki Noda, Takeshi Yoneda, Masashi Masuda, Hisami Okumura, Eiji Takeda, Hiroshi Sakaue, Hironori Yamamoto and Yutaka Taketani : Phosphatemic Index Is a Novel Evaluation Tool for Dietary Phosphorus Load: A Whole-Foods Approach., Journal of Renal Nutrition, Vol.30, No.6, 493-502, 2020. (Tokushima University Institutional Repository) ● Metadata: 114726 (Link to Publication Site) ● Publication site (DOI): 10.1053/j.jrn.2020.02.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32778471 ● Search Scopus @ Elsevier (PMID): 32778471 ● Search Scopus @ Elsevier (DOI): 10.1053/j.jrn.2020.02.005 (Tokushima University Institutional Repository: 114726, DOI: 10.1053/j.jrn.2020.02.005, PubMed: 32778471)
21.	Nobuto Nakanishi, Rie Tsutsumi, Kanako Hara, Takuya Takashima, Emiko Nakataki, Taiga Itagaki, Masafumi Matsuo, Jun Oto and Hiroshi Sakaue : Urinary Titin Is a Novel Biomarker for Muscle Atrophy in Nonsurgical Critically Ill Patients: A Two-Center, Prospective Observational Study., Critical Care Medicine, Vol.2020, No.48(9), 1327-1333, 2020. (Summary) In nonsurgical critically ill patients, urinary titin level increased 10-30 times compared with the normal level. The increased urinary titin level was associated with lower limb muscle atrophy, occurrence of ICU-acquired weakness, and ICU mortality. (Tokushima University Institutional Repository) ● Metadata: 115044 (Link to Publication Site) ● Publication site (DOI): 10.1097/CCM.0000000000004486 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32706557 ● Summary page in Scopus @ Elsevier: 2-s2.0-85089802708 (Tokushima University Institutional Repository: 115044, DOI: 10.1097/CCM.0000000000004486, PubMed: 32706557, Elsevier: Scopus)
22.	Yumiko Miyatake, Yuna Mishima, Rie Tsutsumi, Tamaki Otani, Naoya Suemasa, Saeko Masumoto, Masashi Kuroda and Hiroshi Sakaue : Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging., Biochemical and Biophysical Research Communications, Vol.528, No.3, 499-505, 2020. (Summary) F]-fluoro-2-deoxy-D-glucose (FDG). FDG-PET/CT imaging revealed that insulin administration and exercise load significantly increased FDG accumulation in the skeletal muscle of C57BL/6J mice. FDG accumulation was lower in the skeletal muscle of 14-week-old db/db diabetic model mice exhibiting remarkable insulin resistance compared to that of 7-week-old db/db mice. Based on the continuous observation of FDG accumulation over time in diet-induced obese (DIO) mice, FDG accumulation significantly decreased in 17-week-old mice after the acquisition of insulin resistance. Although insulin-induced glucose uptake in the skeletal muscle was markedly attenuated in 20-week-old DIO mice that had already developed insulin resistance, exercise load effectively increased FDG uptake in the skeletal muscle. Thus, we successfully confirmed that glucose uptake accompanied by insulin administration and exercise load increased in the skeletal muscle using PET-CT. FDG-PET/CT might be an effective tool that could noninvasively capture the chronological changes of metabolic abnormalities in the skeletal muscle of mice. (Tokushima University Institutional Repository) ● Metadata: 118304 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2020.05.165 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32513534 ● Search Scopus @ Elsevier (PMID): 32513534 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.05.165 (Tokushima University Institutional Repository: 118304, DOI: 10.1016/j.bbrc.2020.05.165, PubMed: 32513534)
23.	Nagakatsu Harada, Yuka Gotoda, Adzumi Hatakeyama, Tadahiko Nakagawa, Yumiko Miyatake, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue : Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes., Journal of Muscle Research and Cell Motility, 2020. (Summary) ACTN2 and ACTN3 encode sarcomeric α-actinin-2 and α-actinin-3 proteins, respectively, that constitute the Z-line in mammalian skeletal muscle fibers. In human ACTN3, a nonsense mutation at codon 577 that encodes arginine (R) produces the R577X polymorphism. Individuals having a homozygous 577XX genotype do not produce α-actinin-3 protein. The 577XX genotype reportedly occurs in sprint and power athletes in frequency lower than in the normal population, suggesting that α-actinin-3 deficiency diminishes fast-type muscle function. Among humans who carry 577R alleles, varying ACTN3 expression levels under certain conditions can have diverse effects on atheletic and muscle performance. However, the factors that regulate ACTN3 expression are unclear. Here we investigated whether the unfolded protein response (UPR) under endoplasmic reticulum (ER) stress regulates expression of Actn3 and its isoform Actn2 in mouse C2C12 myotubes. Among UPR-related transcription factors, XBP1 upregulated Actn2, whereas XBP1, ATF4 and ATF6 downregulated Actn3 promoter activity. Chemical induction of ER stress increased Actn2 mRNA levels, but decreased those for Actn3. ER stress also decreased α-actinin-3 protein levels, whereas levels of α-actinin-2 were unchanged. The intracellular composition of muscle contraction-related proteins was altered under ER stress, in that expression of parvalbumin (a fast-twitch muscle-specific protein) and troponin I type 1 (skeletal, slow) was suppressed. siRNA-induced suppression of Actn3 mimicked the inhibitory effect of ER stress on parvalbumin levels. Thus, endogenous expression levels of α-actinin-3 can be altered by ER stress, which may modulate muscle performance and athletic aptitudes, particularly in humans who carry ACTN3 577R alleles. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10974-020-09582-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32451822 ● Search Scopus @ Elsevier (PMID): 32451822 ● Search Scopus @ Elsevier (DOI): 10.1007/s10974-020-09582-7 (DOI: 10.1007/s10974-020-09582-7, PubMed: 32451822)
24.	Masashi Kuroda, Misa Nishiguchi, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Yumiko Miyatake, Mayu Sebe, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription., PLoS ONE, Vol.15, No.5, e0233390, 2020. (Summary) Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity. (Tokushima University Institutional Repository) ● Metadata: 115245 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0233390 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32437400 ● Search Scopus @ Elsevier (PMID): 32437400 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0233390 (Tokushima University Institutional Repository: 115245, DOI: 10.1371/journal.pone.0233390, PubMed: 32437400)
25.	Tetsuya Hosooka, Yusei Hosokawa, Kaku Matsugi, Masakazu Shinohara, Yoko Senga, Yoshikazu Tamori, Chikako Aoki, Sho Matsui, Tsutomu Sasaki, Tadahiro Kitamura, Masashi Kuroda, Hiroshi Sakaue, Kazuhiro Nomura, Kei Yoshino, Yuko Nabatame, Yoshito Itoh, Kanji Yamaguchi, Yoshitake Hayashi, Jun Nakae, Domenico Accili, Takehiko Yokomizo, Susumu Seino, Masato Kasuga and Wataru Ogawa : The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B 4 axis, Proceedings of the National Academy of Sciences of the United States of America, Vol.117, No.21, 11674-11684, 2020. (Summary) Although adipocytes are major targets of insulin, the influence of impaired insulin action in adipocytes on metabolic homeostasis remains unclear. We here show that adipocyte-specific PDK1 (3'-phosphoinositide-dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipose tissue mass. A-PDK1KO mice developed insulin resistance, glucose intolerance, and hepatic steatosis, and this phenotype was suppressed by additional ablation of FoxO1 specifically in adipocytes (A-PDK1/FoxO1KO mice) without an effect on adipose tissue mass. Neither circulating levels of adiponectin and leptin nor inflammatory markers in adipose tissue differed between A-PDK1KO and A-PDK1/FoxO1KO mice. Lipidomics and microarray analyses revealed that leukotriene B4 (LTB4) levels in plasma and in adipose tissue as well as the expression of 5-lipoxygenase (5-LO) in adipose tissue were increased and restored in A-PDK1KO mice and A-PDK1/FoxO1KO mice, respectively. Genetic deletion of the LTB4 receptor BLT1 as well as pharmacological intervention to 5-LO or BLT1 ameliorated insulin resistance in A-PDK1KO mice. Furthermore, insulin was found to inhibit LTB4 production through down-regulation of 5-LO expression via the PDK1-FoxO1 pathway in isolated adipocytes. Our results indicate that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK1-FoxO1 pathway and thereby maintains systemic insulin sensitivity. (Link to Publication Site) ● Publication site (DOI): 10.1073/pnas.1921015117 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32393635 ● Search Scopus @ Elsevier (PMID): 32393635 ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1921015117 (DOI: 10.1073/pnas.1921015117, PubMed: 32393635)
26.	Masashi Masuda, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Yamanaka-Okumura, Hiroshi Sakaue, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b)., The Biochemical Journal, Vol.477, No.4, 817-831, 2020. (Summary) Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Although we previously reported that vitamin A-deficient (VAD) rats had increased urine Pi excretion through the decreased renal expression of Npt2a and Npt2c, the effect of vitamin A on the intestinal Npt2b expression remains unclear. In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. The transcriptional activity of reporter plasmid containing the promoter region of the rat Npt2b gene was reduced by ATRA in NIH3T3 cells overexpressing retinoic acid receptor (RAR) and retinoid X receptor (RXR). On the other hand, CCAAT/enhancer-binding proteins (C/EBP) induced transcriptional activity of the Npt2b gene. Knockdown of the C/EBP gene and a mutation analysis of the C/EBP responsible element in the Npt2b gene promoter indicated that C/EBP plays a pivotal role in the regulation of Npt2b gene transcriptional activity by ATRA. EMSA revealed that the RAR/RXR complex inhibits binding of C/EBP to Npt2b gene promoter. Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene. (Tokushima University Institutional Repository) ● Metadata: 114417 (Link to Publication Site) ● Publication site (DOI): 10.1042/BCJ20190716 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357 ● Search Scopus @ Elsevier (PMID): 32016357 ● Search Scopus @ Elsevier (DOI): 10.1042/BCJ20190716 (Tokushima University Institutional Repository: 114417, DOI: 10.1042/BCJ20190716, PubMed: 32016357)
27.	Masashi Kuroda, Rumi Onoyama, Waka Sasaki, Mayu Sebe, Tadahiro Kitamura, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression., Biochemical and Biophysical Research Communications, Vol.525, No.1, 39-45, 2020. (Summary) Researchers frequently use 3T3-L1 adipocytes as a fat cell line, but the capacity of this line for insulin-mediated glucose transport is lower than that of primary isolated fat cells. In this study, we found that 5-azacytidine (5-aza-C), DNA methyltransferase 1 inhibitor, enhanced insulin-stimulated 2-deoxyglucose (2-DG) transport in 3T3-L1 cells after adipogenic differentiation. We next examined the expression of the genes related to glucose transport and insulin signal transduction. The insulin independent glucose transporter, glucose transporter 1 (GLUT1), showed lower expression in 5-aza-C pre-treated 3T3-L1 adipocytes, than in un-treated control adipocytes, while the expression of insulin dependent transporter GLUT4 remained unchanged. In addition, insulin receptor substrate-1 (IRS-1) was highly expressed in 5-aza-C pre-treated adipocytes. Based on DNA microarray and functional annotation analysis, we noticed that 5-aza-C pretreatment activated the tumor suppressor p53 pathway. We confirmed that in 5-aza-C adipocytes, p53 expression was markedly higher, and the methylation level of CpGs in its promoter region was lower than in un-treated control adipocytes. Moreover, pharmacological inhibition of p53 restored GLUT1 and IRS-1 expression to the same level as in un-treated 3T3-L1 adipocytes, and significantly decreased insulin-mediated 2-DG uptake. These results suggest that glucose transport capacity in adipocytes is influenced by DNA methylation status, and demethylation induced by 5-aza-C increased it possibly through the p53 signaling pathway. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2020.02.038 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32070490 ● Search Scopus @ Elsevier (PMID): 32070490 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.02.038 (DOI: 10.1016/j.bbrc.2020.02.038, PubMed: 32070490)
28.	Taigo Horiguchi, Yumiko Miyake, Keiko Miyoshi, Ayako Tanimura, Hiroko Hagita, Hiroshi Sakaue and Takafumi Noma : Gene-expression profile reveals the genetic and acquired phenotypes of hyperactive mutant SPORTS rad, The Journal of Medical Investigation : JMI, Vol.VOL67, No.NO1,2, 51-61, 2020. (Summary) Spontaneously Running Tokushima Shikoku (SPORTS) rat is a hyperactive rat strain. However, the causative mutation of this phenotype has not yet been identified. To investigate the molecular basis for the unique phenotype of SPORTS rats, we examined gene-expression profiles by microarray analyses. Among adenylate kinase isozymes that maintain the homeostasis of cellular adenine nucleotide composition in the cell, only adenylate kinase 1 is highly up-regulated in both exercised and sedentary SPORTS rats compared with wild-type (WT) rats, 5.5-fold and 3.3-fold, respectively. Further comparative analyses revealed that genes involved in glucose metabolism were up-regulated in skeletal muscle tissue of exercised SPORTS rats compared with sedentary mutants, whereas genes related to extracellular matrix or region were down-regulated compared with WT rats. In brain tissue of sedentary SPORTS rats, genes associated with defense and catecholamine metabolism were highly expressed compared with WT rats. These findings suggest that genetic mutation(s) in SPORTS rat remodels metabolic demands through differentially regulating gene expression regardless of exercise. Therefore, the SPORTS rats are useful animal model not only for further examining the effects of exercise on metabolism but also for deeply studying the molecular basis how mutation affect the psychological motivation with spontaneous voluntary exercise phenotype. J. Med. Invest. 67 : 51-61, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114556 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.51 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378618 ● Search Scopus @ Elsevier (PMID): 32378618 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.51 (Tokushima University Institutional Repository: 114556, DOI: 10.2152/jmi.67.51, PubMed: 32378618)
29.	Nobuto Nakanishi, Rie Tsutsumi, Yoshihiro Okayama, Takuya Takashima, Yoshitoyo Ueno, Taiga Itagaki, Yasuo Tsutsumi, Hiroshi Sakaue and Jun Oto : Monitoring of muscle mass in criticaly ill patients: comparison of ultrasound and two bioelectrical impedance analysis devices, Journal of Intensive Care, Vol.7, 61, 2020. (Summary) Skeletal muscle atrophy commonly occurs in critically ill patients, and decreased muscle mass is associated with worse clinical outcomes. Muscle mass can be assessed using various tools, including ultrasound and bioelectrical impedance analysis (BIA). However, the effectiveness of muscle mass monitoring is unclear in critically ill patients. This study was conducted to compare ultrasound and BIA for the monitoring of muscle mass in critically ill patients. We recruited adult patients who were expected to undergo mechanical ventilation for > 48 h and to remain in the intensive care unit (ICU) for > 5 days. On days 1, 3, 5, 7, and 10, muscle mass was evaluated using an ultrasound and two BIA devices (Bioscan: Malton International, England; Physion: Nippon Shooter, Japan). The influence of fluid balance was also evaluated between each measurement day. We analyzed 93 images in 21 patients. The age of the patients was 69 (interquartile range, IQR, 59-74) years, with 16 men and 5 women. The length of ICU stay was 11 days (IQR, 9-25 days). The muscle mass, monitored by ultrasound, decreased progressively by 9.2% (95% confidence interval (CI), 5.9-12.5%), 12.7% (95% CI, 9.3-16.1%), 18.2% (95% CI, 14.7-21.6%), and 21.8% (95% CI, 17.9-25.7%) on days 3, 5, 7, and 10 ( < 0.01), respectively, with no influence of fluid balance ( = 0.04, = 0.74). The muscle mass did not decrease significantly in both the BIA devices (Bioscan, = 0.14; Physion, = 0.60), and an influence of fluid balance was observed (Bioscan, = 0.37, < 0.01; Physion, = 0.51, < 0.01). The muscle mass assessment at one point between ultrasound and BIA was moderately correlated (Bioscan, = 0.51, < 0.01; Physion, = 0.37, < 0.01), but the change of muscle mass in the same patient did not correlate between these two devices (Bioscan, = - 0.05, = 0.69; Physion, = 0.23, = 0.07). Ultrasound is suitable for sequential monitoring of muscle atrophy in critically ill patients. Monitoring by BIA should be carefully interpreted owing to the influence of fluid change. UMIN000031316. Retrospectively registered on 15 February 2018. (Keyword) ultrasound / Bioelectrical impedance analysis / muscle atrophy (Tokushima University Institutional Repository) ● Metadata: 114541 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40560-019-0416-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31890223 ● Summary page in Scopus @ Elsevier: 2-s2.0-85077117012 (Tokushima University Institutional Repository: 114541, DOI: 10.1186/s40560-019-0416-y, PubMed: 31890223, Elsevier: Scopus)
30.	Shiho Satomi, Atsushi Morio, Hirotsugu Miyoshi, Ryuji Nakamura, Rie Tsutsumi, Hiroshi Sakaue, Toshimichi Yasuda, Noboru Saeki and Yasuo M. Tsutsumi : Branched-chain amino acids-induced cardiac protection against ischemia/reperfusion injury., Life Sciences, Vol.245, 2020. (Summary) BCAA treatment exhibits a protective effect in myocardial I/R injury and that mTOR plays an important role in this preconditioning effect. (Keyword) Amino Acids, Branched-Chain / Animals / Blotting, Western / Cardiotonic Agents / Disease Models, Animal / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Myocardial Reperfusion Injury / Myocytes, Cardiac / Rats / Rats, Wistar / Sirolimus / TOR Serine-Threonine Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2020.117368 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32001270 ● Summary page in Scopus @ Elsevier: 2-s2.0-85078659582 (DOI: 10.1016/j.lfs.2020.117368, PubMed: 32001270, Elsevier: Scopus)
31.	Mayu Sebe, Rie Tsutsumi, Takuro Oyama, T Yousuke Horikawa, Yuta Uemura, Nami Kakuta, Yoko Sakai, Atsushi Morio, Hirotsugu Miyoshi, Takashi Kondo, Tomoaki Urabe, Yuko Noda, Satoshi Kamiya, Noboru Saeki, Masashi Kuroda, Katsuya Tanaka, Yasuo Tsutsumi and Hiroshi Sakaue : Assessment of postoperative nutritional status and physical function between open surgical aortic valve replacement and transcatheter aortic valve implantation in elderly patients., The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 139-144, 2020. (Summary) Background and aims : Severe aortic stenosis (AS) has been normally treated with surgical aortic valve replacement (AVR) whereas recently, transcatheter aortic valve implantation (TAVI) has been introduced as a minimally invasive operation for patients with high surgical risk and frailty. In this study, we have evaluated postoperative physical function and nutrition intake in the patients following AVR and TAVI. Methods : This prospective observational study involved 9 patients with surgical aortic valve replacement (AVR) and 7 patients with transcatheter aortic valve implantation (TAVI). Body composition was measured one day prior surgery, postoperative day (POD) 1, POD 3, POD 5 and POD 7. Hand grip strength, calf circumference and gait speed were measured one day before surgery and on the day of discharge. Results : Skeletal muscle was significantly decreased in AVR patients at postoperative day 3 and 7, while there was no change in TAVI patients. Patients with TAVI showed higher dietary intake after surgery compared to patients with AVR, and they maintained hand grip strength and calf circumference at discharge. Conclusions : In elderly patients with AS, TAVI can improve post-operative recovery maintaining nutritional status and physical function even. J. Med. Invest. 67 : 139-144, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114644 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.139 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378597 ● Search Scopus @ Elsevier (PMID): 32378597 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.139 (Tokushima University Institutional Repository: 114644, DOI: 10.2152/jmi.67.139, PubMed: 32378597)
32.	Tetsuya Shiuchi, Yumiko Miyatake, Airi Otsuka, Sachiko Chikahisa, Hiroshi Sakaue and Hiroyoshi Sei : Role of orexin in exercise-induced leptin sensitivity in the mediobasal hypothalamus of mice., Biochemical and Biophysical Research Communications, Vol.514, No.1, 166-172, 2019. (Summary) Orexin is known as an important neuropeptide in the regulation of energy metabolism. However, the role of orexin in exercise-induced leptin sensitivity in the hypothalamus has been unclear. In this study, we determined the effect of transient treadmill exercise on leptin sensitivity in the mediobasal hypothalamus (MBH) of mice and examined the role of orexin in post-exercise leptin sensitivity. Treadmill running for 45min increased the orexin neuron activity in mice. Intraperitoneal injection of a submaximal dose of leptin after exercise stimulated the phosphorylation of signal transducer and activator of transcription 3 (STAT3) in MBH of mice post-exercise compared with that in non-exercised mice, although intracerebroventricular (icv) injection of leptin did not enhance STAT3 phosphorylation, even after exercise. Icv injection of an orexin receptor antagonist, SB334867 reduced STAT3 phosphorylation, which was enhanced by icv injection of orexin but not by direct injection of orexin into MBH. Exercise increased the phosphorylation of extracellular signal-regulated kinases (ERKs) in the MBH of mice, while ERK phosphorylation was reduced by SB334867. Leptin injection after exercise increased the leptin level in MBH, whereas icv injection of SB334867 suppressed the increase in the leptin level in MBH of mice. These results indicate that the activation of orexin neurons by exercise may contribute to the enhancement of leptin sensitivity in MBH. This effect may be mediated by increased transportation of circulating leptin into MBH, with the involvement of ERK phosphorylation. (Tokushima University Institutional Repository) ● Metadata: 115013 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2019.04.145 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31029425 ● Search Scopus @ Elsevier (PMID): 31029425 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2019.04.145 (Tokushima University Institutional Repository: 115013, DOI: 10.1016/j.bbrc.2019.04.145, PubMed: 31029425)
33.	Masahiro Bando, Saeko Masumoto, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : Effect of olive oil consumption on aging in a senescence-accelerated mice-prone 8 (SAMP8) model., The Journal of Medical Investigation : JMI, Vol.66, No.3.4, 241-247, 2019. (Summary) Background : Mediterranean diets have been linked to a reduced risk of cancer, vascular illnesses, Parkinson's and Alzheimer's disease. Olive oil is the primary fat source in the Mediterranean diet ; however, only a few studies have investigated the effect of olive oil on aging. In the present study, we aimed to determine whether consumption of olive oil significantly influences aging and memory in senescence-accelerated mouse-prone 8 (SAMP8). Methods : SAMP8 and senescence-accelerated mouse resistant 1 (SAMR1) mice were fed either 7% soy oil or 1% olive oil and 6% soy oil during a six-month study period. Reduction in memory in passive avoidance learning was examined after two months from the initiation of the experiment. Results : The weight of organs including the liver, kidney, spleen, and fat tissue changed significantly and memory performance was reduced in SAMP8 than in SAMR1 mice. There were no significant differences in SAMP8 and SAMR1 mice; however, blood triglyceride level decreased significantly in SAMP8 mice fed on olive oil. Conclusions : These results suggest that consuming olive oil may not have a protective role in aging and memory recall, but beneficial effects may be related to improvement in lipid metabolism. J. Med. Invest. 66 : 241-247, August, 2019. (Keyword) aging / Animals / Avoidance Learning / Diet, Mediterranean / memory / Mice / Models, Animal / Olive Oil / Organ Size / Triglycerides (Tokushima University Institutional Repository) ● Metadata: 113365 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656282 ● Summary page in Scopus @ Elsevier: 2-s2.0-85074168190 (Tokushima University Institutional Repository: 113365, DOI: 10.2152/jmi.66.241, PubMed: 31656282, Elsevier: Scopus)
34.	Rie Tsutsumi, 瀬部真由, 別府香名, 渡辺涼乃, 尾平優, Masashi Kuroda and Hiroshi Sakaue : Management of dysgeusia and dysosmia caused by chemotherapy, The Journal of Japanese Society for Parenteral and Enteral Nutrition, Vol.33, No.4, 1019-1024, 2018. (Summary) <p>がんの化学療法中に味覚・嗅覚障害は頻繁に生じ，患者のquality of life(以下，QOLと略)だけでなく，体重低下や栄養状態の悪化を引き起こす深刻な副作用である．しかしながらこれまで確立された治療法や予防策はなく，食事内容や形態の工夫が主な対処法であった．味覚障害は薬剤による亜鉛のキレート化が原因であるとされているが，これに加えて味覚受容体遺伝子の発現変化や口腔粘膜障害の影響も報告されている．本稿では，化学療法中に生じる味覚・嗅覚障害の実態とともに，これに対する栄養的なアプローチを紹介する．</p> (Keyword) 味覚障害 / 嗅覚障害 / 化学療法 (Link to Publication Site) ● Publication site (DOI): 10.11244/jspen.33.1019 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282763059771520 ● Search Scopus @ Elsevier (DOI): 10.11244/jspen.33.1019 (DOI: 10.11244/jspen.33.1019, CiNii: 1390282763059771520)
35.	松島里那, 堤理恵, Hitoshi Shiyouno, 別府香名, 渡辺涼乃, 尾平優, 黒田雅士, Noriaki Takeda and Hiroshi Sakaue : Dysgeusia during cancer treatment and dietary intervention, Shikoku Acta Medica, Vol.74, No.3, 101-106, 2018. (Summary) For patients with cancer, malnutrition is one of the most serious problems. Cancer treatments, such as chemotherapy and radiotherapy, are effective for metastasis and tumor reduction as adjuvant therapy at the perioperative stage, in addition to prolonging the life of a patient and providing a radical cure. On the other hand, loss of appetite that is induced by the above treatment sometimes worsens the nutritional health of a patient. Therefore, it confers prolonged hospitalization and a delay in additional chemotherapy or surgery. Moreover, other side effects besides the loss of appetite due to chemoradiotherapy(hair loss, nausea, vomiting, and diarrhea, among others)can lead to worse nutritional health. Among these side effects, taste disorder is a major factor of decreasing meal intake and is a severe problem occurring frequently during treatment. However, its fundamental reasons, remedial measures, and treatments have not been established yet. In this article, we will report the previous basic research and clinical problems of dysgeusia that occurs during cancer treatment, and introduce a nutritional approach to preventing or improving dysgeusia. (Tokushima University Institutional Repository) ● Metadata: 112298 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050282813469287552 (Tokushima University Institutional Repository: 112298, CiNii: 1050282813469287552)
36.	Nagakatsu Harada, Adzumi Hatakeyama, Maiko Okuyama, Yumiko Miyatake, Tadahiko Nakagawa, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue : Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein., Biochemical and Biophysical Research Communications, Vol.502, No.3, 422-428, 2018. (Summary) expression and thereby induced production of full-length α-actinin-3 protein in the presence of aminoglycoside. Together these results indicate that the ACTN3 R577X polymorphism could be a novel target for readthrough therapy, which may affect athletic and muscle performance in humans. (Keyword) Actinin / Caffeine / Codon, Nonsense / Gentamicins / HEK293 Cells / Humans / Muscle, Skeletal / Mutant Proteins / Peptide Chain Termination, Translational / RNA Stability / RNA, Messenger / Transfection (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2018.05.193 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29857001 ● Search Scopus @ Elsevier (PMID): 29857001 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.05.193 (DOI: 10.1016/j.bbrc.2018.05.193, PubMed: 29857001)
37.	Manami Abe, Yuki Matsuo, Akiko Harada, Takayuki Uchida, Kanako Kitahata, Chisato Tomida, Katsuya Hirasaka, Shigetada Kondo, Nagakatsu Harada, Yutaka Nakaya, Hiroshi Sakaue, Reiko Nakao and Takeshi Nikawa : Distinct Gene Expression Profile Distinguishes Increased Metabolic Activity in Spontaneously Hyperactive Rats While Sedentary from That Induced by Exercise, Advances in Biological Chemistry, Vol.8, No.01, 1-14, 2018. (Tokushima University Institutional Repository) ● Metadata: 111609 (Link to Publication Site) ● Publication site (DOI): 10.4236/abc.2018.81001 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.4236/abc.2018.81001 (Tokushima University Institutional Repository: 111609, DOI: 10.4236/abc.2018.81001)
38.	Chikugo Momoko, Sebe Mayu, Rie Tsutsumi, Iuchi Marina, Jun Kishi, Masashi Kuroda, Nagakatsu Harada, Yasuhiko Nishioka and Hiroshi Sakaue : Effect of Janus kinase inhibition by tofacitinib on body composition and glucose metabolism., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 166-170, 2018. (Summary) Tofacitinib is the first Janus Kinase (JAK) inhibitor to treat moderately to severely active RA. In this study, we investigated whether the effect of tofacitinib have any effects on body composition in mice and female patients with RA. Female C57BL/6 mice fed with a high-fat diet were treated with 30 mg/kg/day tofacitinib or vehicle for 70 days. Following treatment, trunk muscle, subcutaneous fat, and visceral fats were measured using X-ray computed tomography CT scan. Glucose tolerance and insulin sensitivity were assessed. In female RA patients treated with biological disease modified anti-rheumatic-drugs (biological DMARDs) or tofacitinib (n=4 per group), we also evaluated the body composition after 3 months from the start of treatment initiation using bioelectrical impedance analysis. Treatment with tofacitinib did not affect the body weight, and body composition in C57BL/6 mice. It also did not affect glucose, and insulin tolerance in mice. In patients with RA, treatment with biological DMARDs did not affect the body composition whereas the muscle mass was unchanged after receiving tofacitinib and the fat mass was significantly increased. J. Med. Invest. 65:166-170, August, 2018. (Tokushima University Institutional Repository) ● Metadata: 112232 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.166 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282855 ● Search Scopus @ Elsevier (PMID): 30282855 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.166 (Tokushima University Institutional Repository: 112232, DOI: 10.2152/jmi.65.166, PubMed: 30282855)
39.	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. (Link to Publication Site) ● Publication site (DOI): 10.1002/jcb.26031 (Link to Search Site for Scientific Articles) ● 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)
40.	Masato Miyake, Masashi Kuroda, Hiroshi Kiyonari, Kenji Takehana, Satoshi Hisanaga, Masatoshi Morimoto, Jun Zhang, Miho Oyadomari, Hiroshi Sakaue and Seiichi Oyadomari : Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice., PLoS ONE, Vol.12, No.6, e0179955, 2017. (Summary) As a novel model of muscle wasting, HSA-Fv2E-PERK Tg mice provide a convenient tool for studying the pathogenesis of muscle loss and for assessing putative therapeutics. (Tokushima University Institutional Repository) ● Metadata: 114340 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0179955 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28644884 ● Search Scopus @ Elsevier (PMID): 28644884 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0179955 (Tokushima University Institutional Repository: 114340, DOI: 10.1371/journal.pone.0179955, PubMed: 28644884)
41.	Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara : The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes. (Tokushima University Institutional Repository) ● Metadata: 110925 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37739 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917 ● Search Scopus @ Elsevier (PMID): 28502917 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739 (Tokushima University Institutional Repository: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917)
42.	Yutaka Nakaya, Daiju Fukuda, Takashi Oyamada, Kazuo Ogawa, Nagakatsu Harada, Hironori Nakagami, Ryuichi Morishita, Masataka Sata and Hiroshi Sakaue : A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury., The Journal of Medical Investigation : JMI, Vol.64, No.1, 2, 64-67, 2017. (Summary) Although Lp(a) have been thought to be a cardiovascular risk factor, it is unclear whether lowering Lp(a) levels reduces the risk of cardiovascular diseases. No pharmacological agents which selectively reduce serum Lp(a) levels, and Lp(a) is present in primate but absent in common laboratory animals such as mice and pigs. In the present study we used transgenic mice of human Lp(a) and tested effect a novel Lp(a) lowering drug D-47 on neointima formation after vascular injury. D-47 successfully decreased plasma levels of Lp(a) and possibly inhibited neointima formation in Lp(a) transgenic mice. The results indicate that we can modulate plasma Lp(a) levels by pharmacologic agents and inhibit atherogenic properties of Lp(a) by reducing plasma levels of Lp(a). J. Med. Invest. 64: 64-67, February, 2017. (Keyword) lipoprotein a / atherosclerosis / cardiovascular events / low density lipoprotein (Tokushima University Institutional Repository) ● Metadata: 111083 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.64 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373630 ● Search Scopus @ Elsevier (PMID): 28373630 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.64 (Tokushima University Institutional Repository: 111083, DOI: 10.2152/jmi.64.64, PubMed: 28373630)
43.	Yumiko Miyatake, Tetsuya Shiuchi, Kazuaki Mawatari, Satomi Toda, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Masashi Kuroda, Mayu Sebe, Rie Tsutsumi, Nagakatsu Harada, Yasuhiko Minokoshi, Tadahiro Kitamura, Koro Gotoh, Masaki Ueno, Yutaka Nakaya and Hiroshi Sakaue : Intracerebroventricular injection of ghrelin decreases wheel running activity in rats., Peptides, Vol.87, 12-19, 2017. (Summary) There is an increasing interest in elucidating the molecular mechanisms by which voluntary exercise is regulated. In this study, we examined how the central nervous system regulates exercise. We used SPORTS rats, which were established in our laboratory as a highly voluntary murine exercise model. SPORTS rats showed lower levels of serum ghrelin compared with those of the parental line of Wistar rats. Intracerebroventricular and intraperitoneal injection of ghrelin decreased wheel-running activity in SPORTS rats. In addition, daily injection of the ghrelin inhibitor JMV3002 into the lateral ventricles of Wistar rats increased wheel-running activity. Co-administration of obestatin inhibited ghrelin-induced increases in food intake but did not inhibit ghrelin-induced suppression of voluntary exercise in rats. Growth hormone secretagogue receptor (GHSR) in the hypothalamus and hippocampus of SPORTS rats was not difference that in control rats. We created an arcuate nucleus destruction model by administering monosodium glutamate (MSG) to neonatal SPORTS rats. Injection of ghrelin into MSG-treated rats decreased voluntary exercise but did not increase food intake, suggesting that wheel-running activity is not controlled by the arcuate nucleus neurons that regulate feeding. These results provide new insights into the mechanism by which ghrelin regulates voluntary activity independent of arcuate nucleus neurons. (Tokushima University Institutional Repository) ● Metadata: 113364 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.peptides.2016.11.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27825986 ● Summary page in Scopus @ Elsevier: 2-s2.0-84995961350 (Tokushima University Institutional Repository: 113364, DOI: 10.1016/j.peptides.2016.11.005, PubMed: 27825986, Elsevier: Scopus)
44.	Rie Tsutsumi, Hiroshi Sakaue and Masaji Nishimura : ARDS患者に投与すべき熱量はどのように決めるのか?, 救急·集中治療, Vol.29, No.1-2, 125-1313, 2017. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291854812347648 (CiNii: 1520291854812347648)
45.	Zhi-Hong Yang, Masahiro Bando, Toshihiro Sakurai, Ye Chen, Beatrice Emma-Okon, Bree Wilhite, Daiju Fukuda, Boris Vaisman, Milton Pryor, Yoshiyuki Wakabayashi, Maureen Sampson, Zu-Xi Yu, Akiko Sakurai, Abdalrahman Zarzour, Hiroko Miyahara, Jiro Takeo, Hiroshi Sakaue, Masataka Sata and Alan T. Remaley : Long-chain monounsaturated fatty acid-rich fish oil attenuates the development of atherosclerosis in mouse models., Molecular Nutrition & Food Research, Vol.60, No.10, 2208-2218, 2016. (Summary) SCOPE: Fish oil-derived long-chain monounsaturated fatty acids (LCMUFA) containing chain lengths longer than 18 were previously shown to improve cardiovascular disease risk factors in mice. However, it is not known if LCMUFA also exerts anti-atherogenic effects. The main objective of the present study was to investigate the effect of LCMUFA on the development of atherosclerosis in mouse models.METHODS AND RESULTS: LDLR-KO mice were fed Western diet supplemented with 2% (w/w) of either LCMUFA concentrate, olive oil, or not (control) for 12 wk. LCMUFA, but not olive oil, significantly suppressed the development of atherosclerotic lesions and several plasma inflammatory cytokine levels, although there were no major differences in plasma lipids between the three groups. At higher doses 5% (w/w) LCMUFA supplementation was observed to reduce pro-atherogenic plasma lipoproteins and to also reduce atherosclerosis in ApoE-KO mice fed a Western diet. RNA sequencing and subsequent qPCR analyses revealed that LCMUFA upregulated PPAR signaling pathways in liver. In cell culture studies, apoB-depleted plasma from LDLR-K mice fed LCMUFA showed greater cholesterol efflux from macrophage-like THP-1 cells and ABCA1-overexpressing BHK cells.CONCLUSION: Our research showed for the first time that LCMUFA consumption protects against diet-induced atherosclerosis, possibly by upregulating the PPAR signaling pathway. (Keyword) Long-chain monounsaturated / atherosclerosis / PPAR signaling / cholesterol efflux, / inflammation (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.201600142 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27273599 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027917138 (DOI: 10.1002/mnfr.201600142, PubMed: 27273599, Elsevier: Scopus)
46.	Masashi Kuroda, Ayako Tominaga, Kasumi Nakagawa, Misa Nishiguchi, Mayu Sebe, Yumiko Miyatake, Tadahiro Kitamura, Rie Tsutsumi, Nagakatsu Harada, Yutaka Nakaya and Hiroshi Sakaue : DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes., PLoS ONE, Vol.11, No.8, e0160532, 2016. (Summary) Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3T3-L1 adipocytes. Using bisulfite sequencing, we found that CpG islands in the leptin promoter are highly methylated in 3T3-L1cells. 5-azacytidine, an inhibitor of DNA methyltransferase, markedly increased leptin expression as pre-adipocytes matured into adipocytes. Remarkably, leptin expression was stimulated by insulin in adipocytes derived from precursor cells exposed to 5-azacytidine, but suppressed by thiazolidinedione and dexamethasone. In contrast, adipocytes derived from untreated precursor cells were unresponsive to both 5-azacytidine and hormonal stimuli, although lipid accumulation was sufficient to boost leptin expression in the absence of demethylation. Taken together, the results suggest that leptin expression in 3T3-L1 cells requires DNA demethylation prior to adipogenesis, transcriptional activation during adipogenesis, and lipid accumulation after adipogenesis. (Tokushima University Institutional Repository) ● Metadata: 110107 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0160532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27494408 ● Search Scopus @ Elsevier (PMID): 27494408 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0160532 (Tokushima University Institutional Repository: 110107, DOI: 10.1371/journal.pone.0160532, PubMed: 27494408)
47.	Michio Shimabukuro, H Sato, Hirofumi Izaki, Daiju Fukuda, E Uematsu, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Hiro-omi Kanayama, H Masuzaki and Masataka Sata : Depot- and gender-specific expression of NLRP3 inflammasome and toll-like receptors in adipose tissue of cancer patients., BioFactors, Vol.42, No.4, 397-406, 2016. (Keyword) obesity / inflammation / gender (Link to Publication Site) ● Publication site (DOI): 10.1002/biof.1287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27086574 ● Summary page in Scopus @ Elsevier: 2-s2.0-84982113330 (DOI: 10.1002/biof.1287, PubMed: 27086574, Elsevier: Scopus)
48.	Sachiko Nishimoto, Daiju Fukuda, Yasutomi Higashikuni, Kimie Tanaka, Yoichiro Hirata, Chie Murata, Joo-Ri Kim-Kaneyama, Fukiko Sato, Masahiro Bando, Shusuke Yagi, Takeshi Soeki, Tetsuya Hayashi, Issei Imoto, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Obesity-induced DNA released from adipocytes stimulates chronic adipose tissue inflammation and insulin resistance., Science Advances, Vol.2, No.3, e1501332, 2016. (Summary) Obesity stimulates chronic inflammation in adipose tissue, which is associated with insulin resistance, although the underlying mechanism remains largely unknown. Here we showed that obesity-related adipocyte degeneration causes release of cell-free DNA (cfDNA), which promotes macrophage accumulation in adipose tissue via Toll-like receptor 9 (TLR9), originally known as a sensor of exogenous DNA fragments. Fat-fed obese wild-type mice showed increased release of cfDNA, as determined by the concentrations of single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) in plasma. cfDNA released from degenerated adipocytes promoted monocyte chemoattractant protein-1 (MCP-1) expression in wild-type macrophages, but not in TLR9-deficient (Tlr9 (-/-) ) macrophages. Fat-fed Tlr9 (-/-) mice demonstrated reduced macrophage accumulation and inflammation in adipose tissue and better insulin sensitivity compared with wild-type mice, whereas bone marrow reconstitution with wild-type bone marrow restored the attenuation of insulin resistance observed in fat-fed Tlr9 (-/-) mice. Administration of a TLR9 inhibitory oligonucleotide to fat-fed wild-type mice reduced the accumulation of macrophages in adipose tissue and improved insulin resistance. Furthermore, in humans, plasma ssDNA level was significantly higher in patients with computed tomography-determined visceral obesity and was associated with homeostasis model assessment of insulin resistance (HOMA-IR), which is the index of insulin resistance. Our study may provide a novel mechanism for the development of sterile inflammation in adipose tissue and a potential therapeutic target for insulin resistance. (Tokushima University Institutional Repository) ● Metadata: 110123 (Link to Publication Site) ● Publication site (DOI): 10.1126/sciadv.1501332 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27051864 ● Summary page in Scopus @ Elsevier: 2-s2.0-84986905526 (Tokushima University Institutional Repository: 110123, DOI: 10.1126/sciadv.1501332, PubMed: 27051864, Elsevier: Scopus)
49.	Sebe Mayu, Rie Tsutsumi, Yamaguchi Sotaro, Horikawa T. Yousuke, Harada Nagakatsu, Takuro Oyama, Nami Kakuta, Katsuya Tanaka, Yasuo Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue : The synergistic effects of omega-3 fatty acids against 5-fluorouracil-induced mucosal impairment in mice., BMC Nutrition, Vol.2, No.17, 1-10, 2016. (Tokushima University Institutional Repository) ● Metadata: 114371 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40795-016-0057-7 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1186/s40795-016-0057-7 (Tokushima University Institutional Repository: 114371, DOI: 10.1186/s40795-016-0057-7)
50.	Maerjianghan Abuduli, Hirokazu Ohminami, Tamaki Otani, Hitoshi Kubo, Haruka Ueda, Yoshichika Kawai, Masashi Masuda, Hisami Okumura, Hiroshi Sakaue, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : Effects of dietary phosphate on glucose and lipid metabolism., American Journal of Physiology, Endocrinology and Metabolism, Vol.310, No.7, E526-E538, 2016. (Summary) Recent epidemiological and animal studies have suggested that excess intake of phosphate (Pi) is a risk factor for the progression of chronic kidney disease and its cardiovascular complications. However, little is known about the impact of dietary high Pi intake on the development of metabolic disorders such as obesity and type II diabetes. In this study, we investigated the effects of dietary Pi on glucose and lipid metabolism in healthy rats. Male, 8-wk-old Sprague-Dawley rats were divided into 3 groups and given experimental diets containing varying amounts of Pi, i.e. 0.2% (low Pi, LP), 0.6% (control Pi, CP), and 1.2% (high Pi, HP). After 4 weeks, HP group showed lower visceral fat accumulation compared with other groups, accompanied by a low respiratory exchange ratio (VCO2/VO2) without alteration of locomotive activity. HP group had lower levels of plasma insulin and non-esterified fatty acids. In addition, HP group also showed suppressed expression of hepatic lipogenic genes including sterol regulatory element binding protein-1c, fatty acid synthase, and acetyl-CoA carboxylase, whereas there was no difference in hepatic fat oxidation among the groups. On the other hand, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator alpha (PGC1) expression were significantly increased in the brown adipose tissue (BAT) of HP group. Our data demonstrated that a high Pi diet can negatively regulate lipid synthesis in the liver, and increased mRNA expression related to lipid oxidation and UCP1 in BAT, thereby preventing visceral fat accumulation. Thus, dietary Pi is a novel metabolic regulator. (Tokushima University Institutional Repository) ● Metadata: 109976 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00234.2015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26786774 ● Search Scopus @ Elsevier (PMID): 26786774 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00234.2015 (Tokushima University Institutional Repository: 109976, DOI: 10.1152/ajpendo.00234.2015, PubMed: 26786774)
51.	Otsuka Ryo, Nagakatsu Harada, Aoki Shouhei, Shirai Kanna, Kazuchika Nishitsuji, Nozaki Ayane, Hatakeyama Adzumi, Masayuki Shono, Noriko Mizusawa, Katsuhiko Yoshimoto, Yutaka Nakaya, Hiroshi Kitahata and Hiroshi Sakaue : C-terminal region of GADD34 regulates eIF2alpha dephosphorylation and cell proliferation in CHO-K1 cells., Cell Stress & Chaperones, Vol.21, No.1, 29-40, 2016. (Summary) GADD34 is a member of a growth arrest and DNA damage (GADD)-inducible gene family. Here, we established a novel Chinese hamster ovary (CHO)-K1-derived cell line, CHO-K1-G34M, which carries a nonsense mutation (termed the Q525X mutation) in the GADD34 gene. The Q525X mutant protein lacks the C-terminal 66 amino acids required for GADD34 to bind to and activate protein phosphatase 1 (PP1). We investigated the effects of GADD34 with or without the Q525X mutation on the phosphorylation status of PP1 target proteins, including the subunit of eukaryotic initiation factor 2 (eIF2) and glycogen synthase kinase 3 (GSK3). CHO-K1-G34M cells had higher levels of eIF2 phosphorylation compared to the control CHO-K1-normal cells both in the presence and absence of endoplasmic reticulum stress. Overexpression of the wild-type GADD34 protein in CHO-K1-normal cells largely reduced eIF2 phosphorylation, while overexpression of the Q525X mutant did not produce similar reductions. Meanwhile, neither wild type nor Q525X mutation of GADD34 affected the GSK3 phosphorylation status. GADD34 also did not affect the canonical Wnt signaling pathway downstream of GSK3. Cell proliferation rates were higher, while expression levels of the cyclin-dependent kinase inhibitor p21 were lower in CHO-K1-G34M cells compared to the CHO-K1-normal cells. The GADD34 Q525X mutant had a reduced ability to inhibit cell proliferation and enhance p21 expression of the CHO-K1-normal cells compared to the wild-type GADD34 protein. These results suggest that the GADD34 protein C-terminal plays important roles in regulating not only eIF2 dephosphorylation but also cell proliferation in CHO-K1 cells. (Tokushima University Institutional Repository) ● Metadata: 110106 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12192-015-0633-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26318739 ● Summary page in Scopus @ Elsevier: 2-s2.0-84951905379 (Tokushima University Institutional Repository: 110106, DOI: 10.1007/s12192-015-0633-9, PubMed: 26318739, Elsevier: Scopus)
52.	Yumiko Miyatake, Tetsuya Shiuchi, Tomoyo Ueta, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Tadahiro Kitamura, Rie Tsutsumi, Nagakatsu Harada, Yutaka Nakaya and Hiroshi Sakaue : Intracerebroventricular injection of adiponectin regulates locomotor activity in rats, The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 199-203, 2015. (Summary) Enhancing exercise motivation is the best way to prevent obesity and diabetes. In this study, we examined whether adiponectin affects locomotion activity in Wister and Spontaneously-Running Tokushima-Shikoku (SPORTS) rats using two types of behavioral assays: home cage and wheel running activity. SPORTS rats were established from an original line from Wister strain that had shown high level of wheel running activity in our laboratory. Injection of adiponectin into the lateral ventricle of Wister rats and SPORTS rats decreased home cage activity, but no change was observed in the food intake and oxygen consumption. This result indicates the possibility that adiponectin can reduce non-exercise activity thermogenesis (NEAT) and physical activity via the central nervous system. In contrast, injection of adiponectin did not change wheel running activity in SPORTS rats. We produced hypothalamus-destructed model rat using monosodium glutamate (MSG) to elucidate the regulation site of adiponectin. Injection of adiponectin into MSG-treated SPORTS rats did not change amount of home cage activity and food intake, suggesting that adiponectin action on home cage activity was in the hypothalamic area. These results suggest that adiponectin regulates locomotion activity through mediobasal hypothalamus. (Tokushima University Institutional Repository) ● Metadata: 111279 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.62.199 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399348 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942037938 (Tokushima University Institutional Repository: 111279, DOI: 10.2152/jmi.62.199, PubMed: 26399348, Elsevier: Scopus)
53.	Rie Tsutsumi, Tomomi Yoshida, Yoshitaka Nii, Naoki Okahisa, Shinya Iwata, Masao Tsukayama, Rei Hashimoto, Yasuko Taniguchi, Hiroshi Sakaue, Toshio Hosaka, Emi Shuto and Tohru Sakai : Sudachitin, a polymethoxylated flavone, improves glucose and lipid metabolism by increasing mitochondrial biogenesis in skeletal muscle., Nutrition & Metabolism, Vol.11, 32, 2014. (Summary) Obesity is a major risk factor for insulin resistance, type 2 diabetes, and stroke. Flavonoids are effective antioxidants that protect against these chronic diseases. In this study, we evaluated the effects of sudachitin, a polymethoxylated flavonoid found in the skin of the Citrus sudachi fruit, on glucose, lipid, and energy metabolism in mice with high-fat diet-induced obesity and db/db diabetic mice. In our current study, we show that sudachitin improves metabolism and stimulates mitochondrial biogenesis, thereby increasing energy expenditure and reducing weight gain. C57BL/6 J mice fed a high-fat diet (40% fat) and db/db mice fed a normal diet were treated orally with 5 mg/kg sudachitin or vehicle for 12 weeks. Following treatment, oxygen expenditure was assessed using indirect calorimetry, while glucose tolerance, insulin sensitivity, and indices of dyslipidemia were assessed by serum biochemistry. Quantitative polymerase chain reaction was used to determine the effect of sudachitin on the transcription of key metabolism-regulating genes in the skeletal muscle, liver, and white and brown adipose tissues. Primary myocytes were also prepared to examine the signaling mechanisms targeted by sudachitin in vitro. Sudachitin improved dyslipidemia, as evidenced by reduction in triglyceride and free fatty acid levels, and improved glucose tolerance and insulin resistance. It also enhanced energy expenditure and fatty acid β-oxidation by increasing mitochondrial biogenesis and function. The in vitro assay results suggest that sudachitin increased Sirt1 and PGC-1α expression in the skeletal muscle. Sudachitin may improve dyslipidemia and metabolic syndrome by improving energy metabolism. Furthermore, it also induces mitochondrial biogenesis to protect against metabolic disorders. (Link to Publication Site) ● Publication site (DOI): 10.1186/1743-7075-11-32 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25114710 ● Search Scopus @ Elsevier (PMID): 25114710 ● Search Scopus @ Elsevier (DOI): 10.1186/1743-7075-11-32 (DOI: 10.1186/1743-7075-11-32, PubMed: 25114710)
54.	Kazuaki Mawatari, Emiko Yoshioka, Satomi Toda, Sonoko Yasui, Hiroko Furukawa, Takaaki Shimohata, Takamasa Ohnishi, Masaki Morishima, Nagakatsu Harada, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : Enhancement of endothelial function inhibits left atrial thrombi development in an animal model of spontaneous left atrial thrombosis., Circulation Journal, Vol.78, No.8, 1980-1988, 2014. (Summary) Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats. They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980-1988). (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-13-1398 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24859498 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905043629 (DOI: 10.1253/circj.CJ-13-1398, PubMed: 24859498, Elsevier: Scopus)
55.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yoji Hoshina, Kana Kato, Hitoshi Shirakawa, Hiroshi Sakaue, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation., PLoS ONE, Vol.9, No.4, e93856, 2014. (Summary) It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue. (Keyword) Adipocytes / Animals / Blotting, Western / Chemokine CCL2 / DNA Primers / Diabetes Mellitus, Type 2 / Gene Deletion / Glucagon-Like Peptide 1 / Glucose Tolerance Test / Hypoxia-Inducible Factor 1, alpha Subunit / Immunohistochemistry / Insulin / Mice / Mice, Knockout / Real-Time Polymerase Chain Reaction / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0093856 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899440448 (DOI: 10.1371/journal.pone.0093856, PubMed: 24705496, Elsevier: Scopus)
56.	Hirata Yoichiro, Hirotsugu Kurobe, Nishio Chika, Tanaka Kimie, Daiju Fukuda, Uematsu Etsuko, Nishimoto Sachiko, Takeshi Soeki, Nagakatsu Harada, Hiroshi Sakaue, Tetsuya Kitagawa, Michio Shimabukuro, Yutaka Nakaya and Masataka Sata : Exendin-4, a glucagon-like peptide-1 receptor agonist, attenuates neointimal hyperplasia after vascular injury., European Journal of Pharmacology, Vol.699, No.1-3, 106-111, 2013. (Summary) Exendin-4 is a glucagon-like peptide-1 receptor agonist that has been used as a drug for treatment of type 2 diabetes. To investigate the effect of exendin-4 on the cardiovascular system, we investigated the impact of exendin-4 on neointimal hyperplasia of the femoral artery after vascular injury. We performed wire-mediated endovascular injury in C57BL/6 mice, followed by administration of exendin-4 24 nmol/kg/day via infusion pump. Four weeks after the injury, exendin-4 treatment significantly attenuated neointimal hyperplasia of the injured artery, although it did not affect glucose metabolism and lipid profile in wild-type mice. Immunofluorescence study revealed abundant expression of GLP-1 receptor on α-smooth muscle actin-positive cells in the injured vessel. Cell proliferation assay using rat aortic smooth muscle cells showed that exendin-4 reduced PDGF-BB induced smooth muscle cell proliferation through the cAMP/PKA pathway. Exendin-4 also inhibited TNFα production by peritoneal macrophages in response to inflammatory stimulus. Our findings indicate that a GLP-1 receptor agonist attenuated neointimal formation after vascular injury. GLP-1 receptor agonists or drugs that raise endogenous GLP-1 level might be effective in the treatment of vascular diseases. (Keyword) Exendin-4 / GLP-1 / endovascular injury / neointimal hyperplasia / diabetes mellitus (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2012.11.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23220706 ● Search Scopus @ Elsevier (PMID): 23220706 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.11.057 (DOI: 10.1016/j.ejphar.2012.11.057, PubMed: 23220706)
57.	Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Hirata Yoichiro, Hirotsugu Kurobe, Maeda Norikazu, Hiroshi Sakaue, Masuzaki Hiroaki, Shimomura Iichiro and Masataka Sata : Telmisartan ameliorates insulin sensitivity by activating the AMPK/SIRT1 pathway in skeletal muscle of obese db/db mice., Cardiovascular Diabetology, Vol.11, No.1, 139, 2012. (Summary) Telmisartan is a well-established angiotensin II type 1 receptor blocker that improves insulin sensitivity in animal models of obesity and insulin resistance, as well as in humans. Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) γ, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1). Here, we investigated the pathways through which telmisartan acts on skeletal muscle, in vitro as well as in vivo. Nine-week-old male db/db mice were fed a 60% high-fat diet, with orally administrated either vehicle (carboxymethyl-cellulose, CMC), 5 mg/kg telmisartan, or 5 mg/kg telmisartan and 1 mg/kg GW9662, a selective irreversible antagonist of PPARγ, for 5 weeks. Effects of telmisartan on Sirt1 mRNA, AMPK phosphorylation, and NAD+/NADH ratio were determined in C2C12 cultured myocytes. Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4. Our results indicate that telmisartan acts through a PPARγ-independent pathway, but at least partially exerts its effects by acting directly on skeletal muscle AMPK/SIRT1 pathways. (Keyword) AMP-Activated Protein Kinases / Adipocytes / Administration, Oral / Angiotensin II Type 1 Receptor Blockers / Anilides / Animals / Benzimidazoles / Benzoates / Cell Line / Diabetes Mellitus / Diet, High-Fat / Disease Models, Animal / Dose-Response Relationship, Drug / Enzyme Activation / Fatty Acid Transport Proteins / Glucose Transporter Type 4 / Hypertrophy / Insulin / Islets of Langerhans / Male / Mice / Muscle Fibers, Skeletal / Muscle, Skeletal / NAD / Obesity / PPAR gamma / Phosphorylation / RNA, Messenger / Signal Transduction / Sirtuin 1 / Time Factors / Trans-Activators (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2840-11-139 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23137106 ● Search Scopus @ Elsevier (PMID): 23137106 ● Search Scopus @ Elsevier (DOI): 10.1186/1475-2840-11-139 (DOI: 10.1186/1475-2840-11-139, PubMed: 23137106)
58.	Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Yoichiro Hirata, Hirotsugu Kurobe, Hiroshi Sakaue, Yutaka Nakaya, Hiroaki Masuzaki and Masataka Sata : Activation of AMPK-Sirt1 pathway by telmisartan in white adipose tissue: A possible link to anti-metabolic effects., European Journal of Pharmacology, Vol.692, No.1-3, 84-90, 2012. (Summary) Telmisartan exerts anti-metabolic effects beyond its angiotensin receptor blockade activities, but the mechanisms have hitherto remained elusive. We sought to elucidate the peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent and PPAR-γ-independent mechanisms underlying the anti-metabolic effects of telmisartan in white adipose tissue. Nine-week-old male C57BL/6 mice were fed with a 60% high-fat diet for 6 weeks, with 1mg/kg telmisartan or vehicle administrated orally during the last 3 weeks. 3T3-L1 adipocytes were cultured with telmisartan either with 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective irreversible antagonist of PPAR-γ, or compound C, an ATP-competitive inhibitor of AMPK. Western blotting and semiquantitative RT-PCR analysis were used to assess adiponectin, Sirt1, and AMPK levels. Lipid accumulation was assessed by Oil red O staining. The activation of transcription factor PPAR-γ2 was evaluated by using a luciferase reporter assay for mPPAR-γ2 expression plasmid vector. Treatment with telmisartan increased serum adiponectin levels in high-fat diet-fed mice concomitantly with an upregulation of adiponectin mRNA in visceral adipose tissue. In vitro telmisartan treatment dose-dependently increased adiponectin mRNA in 3T3-L1 cells; the increase was inhibited by compound C, but not by GW9662. Telmisartan increased expression of Sirt1 mRNA and Sirt1 protein as well as the phosphorylation of AMPK in 3T3-L1 cells. Telmisartan can increase adiponectin production in white adipose tissue partly via a PPAR-γ2-independent mechanism. Precise understanding of this molecular mechanism will require further investigation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2012.07.026 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22819702 ● Search Scopus @ Elsevier (PMID): 22819702 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.07.026 (DOI: 10.1016/j.ejphar.2012.07.026, PubMed: 22819702)
59.	Nagakatsu Harada, Fujimoto Erika, Okuyama Maiko, Hiroshi Sakaue and Yutaka Nakaya : Identification and functional characterization of human glycerol-3-phosphate acyltransferase 1 gene promoters., Biochemical and Biophysical Research Communications, Vol.423, No.1, 128-133, 2012. (Summary) Glycerol-3-phosphate acyltransferase 1 (GPAT1) acts as a rate limiting enzyme in triacylglycerol and phospholipid synthesis in mammals. GPAT1 regulates hepatic lipid accumulation associated with metabolic disorders. Here we have identified two transcriptional initiation sites and two promoters (promoter I and II) required for expression of the human GPAT1 (hGPAT1) gene. Promoter I regulates transcription of three alternative hGPAT1 mRNA variants, hGPAT1-V1, V2, and V3, while promoter II induces expression of a fourth variant, hGPAT1-V4. RT-PCR analysis and luciferase reporter assays revealed that promoter II acts in lipogenic tissues like the liver (and liver-derived HepG2 cells), whereas promoter I is differentially regulated and also acts in non-liver HeLa cells. Among liver-enriched transcription factors, HNF4α and C/EBPα slightly activated hGPAT1 promoter I, while factors including HNF1α altered promoter II activity. The lipogenic transcription factor SREBP1c greatly increased promoter II activity in HepG2 cells. The use of various truncated or mutated fragments of promoter II revealed that one sterol regulatory element-like motif and one inverted CCAAT box on promoter II contributed to the SREBP1c response. These cis-acting elements and trans-acting factors can be potential targets for manipulation of hepatic GPAT1 levels in humans. (Keyword) Animals / Binding Sites / CCAAT-Enhancer-Binding Proteins / Exons / Glycerol-3-Phosphate O-Acyltransferase / HeLa Cells / Hep G2 Cells / Hepatocyte Nuclear Factor 4 / Humans / Introns / Liver / Mice / NIH 3T3 Cells / Promoter Regions, Genetic / RNA, Messenger / Response Elements / Sterol Regulatory Element Binding Protein 1 / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2012.05.094 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22634312 ● Search Scopus @ Elsevier (PMID): 22634312 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2012.05.094 (DOI: 10.1016/j.bbrc.2012.05.094, PubMed: 22634312)
60.	Hiroshi Sakaue : Insights into Energy Expenditure during Exercise, Journal of the The Japan Diabetes Society, Vol.55, No.5, 306-308, 2012. (Link to Publication Site) ● Publication site (DOI): 10.11213/tonyobyo.55.306 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204907064064 ● Summary page in Scopus @ Elsevier: 2-s2.0-84862578603 (DOI: 10.11213/tonyobyo.55.306, CiNii: 1390001204907064064, Elsevier: Scopus)
61.	Nakagawa Tadahiko, Nagakatsu Harada, Miyamoto Aiko, Kawanishi Yukiko, Yoshida Masaki, Masayuki Shono, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : Membrane topology of murine glycerol-3-phosphate acyltransferase 2., Biochemical and Biophysical Research Communications, Vol.418, No.3, 506-511, 2012. (Summary) Glycerol-3-phosphate acyltransferase (GPAT) is a rate-limiting enzyme in mammalian triacylglycerol biosynthesis. GPAT is a target for the treatment of metabolic disorders associated with high lipid accumulation. Although the molecular basis for GPAT1 activation has been investigated extensively, the activation of other isoforms, such as GPAT2, is less well understood. Here the membrane topology of the GPAT2 protein was examined using an epitope-tag-based method. Exogenously expressed GPAT2 protein was present in the membrane fraction of transformed HEK293 cells even in the presence of Na(2)CO(3) (100 mM), indicating that GPAT2 is a membrane-bound protein. Trypsin treatment of the membrane fraction degraded the N-terminal (FLAG) and C-terminal (myc-epitope) protein tags of the GPAT2 protein. Bioinformatic analysis of the GPAT2 protein sequence indicated four hydrophobic sequences as potential membrane-spanning regions (TM1-TM4). Immunoblotting of the myc-epitope tag, which was inserted between each TM region of the GPAT2 protein, showed that the amino acid sequence between TM3 and TM4 was protected from trypsin digestion. These results suggest that the GPAT2 protein has two transmembrane segments and that the N-terminal and C-terminal regions of this protein face the cytoplasm. These results also suggest that the enzymatically active motifs I-III of the GPAT2 protein face the cytosol, while motif IV is within the membrane. It is expected that the use of this topological model of GPAT2 will be essential in efforts to elucidate the molecular mechanisms of GPAT2 activity in mammalian cells. (Keyword) Amino Acid Motifs / Animals / Cell Membrane / Cytoplasm / Glycerol-3-Phosphate O-Acyltransferase / HEK293 Cells / Humans / Mice / Molecular Sequence Data / Protein Structure, Tertiary (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2012.01.055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22285183 ● Search Scopus @ Elsevier (PMID): 22285183 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2012.01.055 (DOI: 10.1016/j.bbrc.2012.01.055, PubMed: 22285183)
62.	Kazuhito Tawaramoto, Ko Kotani, Mitsuru Hashiramoto, Yukiko Kanda, Tomoki Nagare, Hiroshi Sakaue, Wataru Ogawa, Noriaki Emoto, Masashi Yanagisawa, Tetsuo Noda, Masato Kasuga and Kohei Kaku : Ablation of 3-phosphoinositide-dependent protein kinase 1 (PDK1) in vascular endothelial cells enhances insulin sensitivity by reducing visceral fat and suppressing angiogenesis., Molecular Endocrinology, Vol.26, No.1, 95-109, 2011. (Summary) The phosphatidylinositol 3-kinase signaling pathway in vascular endothelial cells is important for systemic angiogenesis and glucose metabolism. In this study, we addressed the precise role of the 3-phosphoinositide-dependent protein kinase 1 (PDK1)-regulated signaling network in endothelial cells in vivo, using vascular endothelial PDK1 knockout (VEPDK1KO) mice. Surprisingly, VEPDK1KO mice manifested enhanced glucose tolerance and whole-body insulin sensitivity due to suppression of their hepatic glucose production with no change in either peripheral glucose disposal or even impaired vascular endothelial function at 6 months of age. When mice were fed a standard diet at 6 months of age and a high-fat diet at 3 months of age, hypertrophy of epididymal adipose tissues was inhibited, adiponectin mRNA was significantly increased, and mRNA of MCP1, leptin, and TNF was decreased in the white adipose tissue of VEPDK1KO mice in comparison with controls. Consequently, both the circulating adiponectin levels and the activity of hepatic AMP-activated protein kinase were significantly increased, subsequently enhancing whole-body insulin sensitivity and energy expenditure with increased hepatic fatty acid oxidation in VEPDK1KO mice. These results provide the first in vivo evidence that lowered angiogenesis through the deletion of PDK1 signaling not only interferes with the growth of adipose tissue but also induces increased energy expenditure due to amelioration of the adipocytokine profile. This demonstrates an unexpected role of PDK1 signaling in endothelial cells on the maintenance of proper glucose homeostasis through the regulation of adipocyte development. (Keyword) Adiponectin / Adipose Tissue, White / Animals / Chemokine CCL2 / Endothelial Cells / glucose / insulin resistance / Intra-Abdominal Fat / Leptin / Lipid Metabolism / Liver / male / Mice / knockout mice / Neovascularization, Physiologic / obesity / Phosphatidylinositol 3-Kinase / Protein-Serine-Threonine Kinases / RNA, Messenger / signal transduction / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1210/me.2010-0412 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22108800 ● Search Scopus @ Elsevier (PMID): 22108800 ● Search Scopus @ Elsevier (DOI): 10.1210/me.2010-0412 (DOI: 10.1210/me.2010-0412, PubMed: 22108800)
63.	田中佑佳, 杉野博崇, Hideki Nakanishi, Nagakatsu Harada, Hiroshi Sakaue and Yutaka Nakaya : 褥瘡患者において血清アルブミン値は栄養状態を表す良い指標か?, The Journal of Metabolism and Clinical Nutrition, Vol.14, No.1, 9-15, 2011. (Keyword) アルブミン / 褥瘡 / 栄養状態 / 栄養リスク / inflammation (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570572700067958784 (CiNii: 1570572700067958784)
64.	Yutaka Nakaya, Takaaki Shimohata, Sayaka Haraguchi, Toshiyuki Nakao, Jun Minaguchi, Haruo Sumitani, Nagakatsu Harada and Hiroshi Sakaue : Severe catabolic state after an overnight fast in patients with chronic renal failure., Nutrition, Vol.27, No.3, 329-332, 2011. (Summary) Starvation causes more rapid development of a catabolic state in patients with liver cirrhosis than in normal subjects. Because the kidneys have a gluconeogenic activity similar to that of the liver, we tested whether patients with chronic renal failure develop a catabolic state after an overnight fast. The effect of an overnight fast on diurnal changes in respiratory quotient (RQ) was studied in 12 normal subjects and 12 patients with stable chronic renal failure. Changes in RQ in the early morning after an overnight fast were also studied in 27 patients with chronic renal failure not on dialysis. We also examined the effect on RQ of consuming a light snack in the evening before the measurements. The RQ before breakfast, but not at other times, was significantly lower in patients with renal failure than in normal subjects (0.824 ± 0.051 versus 0.868 ± 0.038, P < 0.05). This indicated that patients with renal failure had higher fat use and developed a catabolic state early in the morning. The RQ before breakfast showed significant inverse correlations with creatinine levels (r = -0.604, P < 0.001). Supplementation with a carbohydrate-rich snack in the evening resulted in a significant increase of 0.07 ± 0.04 (P < 0.05) in mean RQ in the early morning. This suggested that a late evening snack is useful for improving the catabolic state of patients with renal failure. Starvation involving an overnight fast facilitates catabolism of visceral and muscle proteins in renal failure. This suggests that nutritional management of renal failure should focus not only on the contents of a meal, but also on the timing of the meal. (Keyword) Aged / Carbon Dioxide / Creatinine / Dietary Carbohydrates / Energy Metabolism / Fasting / Female / Humans / Kidney Failure, Chronic / Lipid Metabolism / Male / Middle Aged / Oxygen Consumption / Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nut.2010.04.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21167682 ● Search Scopus @ Elsevier (PMID): 21167682 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nut.2010.04.008 (DOI: 10.1016/j.nut.2010.04.008, PubMed: 21167682)
65.	Yohko Hirata, Toshio Hosaka, Takeo Iwata, Le Thi Kim Chung, Bayasgalan Jambaldorj, Kiyoshi Teshigawara, Nagakatsu Harada, Hiroshi Sakaue, Tohru Sakai, Katsuhiko Yoshimoto and Yutaka Nakaya : Vimentin binds IRAP and is involved in GLUT4 vesicle trafficking., Biochemical and Biophysical Research Communications, Vol.405, No.1, 96-101, 2011. (Summary) Insulin-responsive aminopeptidase (IRAP) and GLUT4 are two major cargo proteins of GLUT4 storage vesicles (GSVs) that are translocated from a postendosomal storage compartment to the plasma membrane (PM) in response to insulin. The cytoplasmic region of IRAP is reportedly involved in retention of GSVs. In this study, vimentin was identified using the cytoplasmic domain of IRAP as bait. The validity of this interaction was confirmed by pull-down assays and immunoprecipitation in 3T3-L1 adipocytes. In addition, it was shown that GLUT4 translocation to the PM by insulin was decreased in vimentin-depleted adipocytes, presumably due to dispersing GSVs away from the cytoskeleton. These findings suggest that the IRAP binding protein, vimentin, plays an important role in retention of GSVs. (Keyword) 3T3-L1 Cells / Animals / Cystinyl Aminopeptidase / Cytoplasmic Vesicles / Gene Knockdown Techniques / Glucose Transporter Type 4 / Mice / Protein Transport / Vimentin (Tokushima University Institutional Repository) ● Metadata: 113298 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2010.12.134 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21216232 ● Search Scopus @ Elsevier (PMID): 21216232 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2010.12.134 (Tokushima University Institutional Repository: 113298, DOI: 10.1016/j.bbrc.2010.12.134, PubMed: 21216232)
66.	Masaki Yoshida, Nagakatsu Harada, Keiko Yoshida, Tadahiko Nakagawa, Takaaki Shimohata, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : High density lipoprotein inhibits the activation of sterol regulatory element-binding protein-1 in cultured cells., FEBS Letters, Vol.584, No.6, 1217-1222, 2010. (Summary) A link between cellular uptake of high density lipoprotein (HDL) and regulation of sterol regulatory element-binding protein-1 (SREBP-1) was investigated in vitro. HDL decreased nuclear SREBP-1 levels as well as SREBP-1 target gene expression in HepG2 and HEK293 cells. However, HDL did not repress an exogenously expressed, constitutively active form of SREBP-1. HDL increased cellular cholesterol levels, and cellular cholesterol depletion by methyl-beta-cyclodextrin abolished the effects of HDL. These results suggest that HDL inhibits the activation of SREBP-1 through a cholesterol-dependent mechanism, which may play an important role in regulating lipid synthetic pathways mediated by SREBP-1. (Keyword) Acetyl-CoA Carboxylase / Animals / Cells, Cultured / Fatty Acid Synthetase Complex / Gene Expression Regulation, Enzymologic / Hep G2 Cells / Humans / Lipid Metabolism / Lipoproteins, HDL / Male / Promoter Regions, Genetic / Rats / Rats, Sprague-Dawley / Stearoyl-CoA Desaturase / Sterol Regulatory Element Binding Protein 1 / Transcriptional Activation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.febslet.2010.02.034 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20171215 ● Summary page in Scopus @ Elsevier: 2-s2.0-77950369388 (DOI: 10.1016/j.febslet.2010.02.034, PubMed: 20171215, Elsevier: Scopus)
67.	Shintaro Yasue, Hiroaki Masuzaki, Sadanori Okada, Takako Ishii, Chisayo Kozuka, Tomohiro Tanaka, Junji Fujikura, Ken Ebihara, Kiminori Hosoda, Akemi Katsurada, Naro Ohashi, Maki Urushihara, Hiroyuki Kobori, Naoki Morimoto, Takeshi Kawazoe, Motoko Naitoh, Mitsuru Okada, Hiroshi Sakaue, Shigehiko Suzuki and Kazuwa Nakao : Adipose tissue-specific regulation of angiotensinogen in obese humans and mice: impact of nutritional status and adipocyte hypertrophy., American Journal of Hypertension, Vol.23, No.4, 425-431, 2010. (Summary) BACKGROUND: The adipose tissue renin-angiotensin system (RAS) has been implicated in the pathophysiology of obesity and dysfunction of adipose tissue. However, neither regulation of angiotensinogen (AGT) expression in adipose tissue nor secretion of adipose tissue-derived AGT has been fully elucidated in humans. METHODS: Human subcutaneous abdominal adipose tissue (SAT) biopsies were performed for 46 subjects with a wide range of body mass index (BMI). Considering the mRNA level of AGT and indices of body fat mass, the amount of adipose tissue-derived AGT secretion (A-AGT-S) was estimated. Using a mouse model of obesity and weight reduction, plasma AGT levels were measured with a newly developed enzyme-linked immunosorbent assay (ELISA), and the contribution of A-AGT-S to plasma AGT levels was assessed. RESULTS: A-AGT-S was substantially increased in obese humans and the value was correlated with the plasma AGT level in mice. A-AGT-S and plasma AGT were higher in obese mice, whereas lower in mice with weight reduction. However, the AGT mRNA levels in the liver, kidney, and aorta were not altered in the mouse models. In both humans and mice, the AGT mRNA levels in mature adipocytes (MAs) were comparable to those in stromal-vascular cells. Coulter Multisizer analyses revealed that AGT mRNA levels in the MAs were inversely correlated with the average size of mature adipocytes. CONCLUSIONS: This study demonstrates that adipose tissue-derived AGT is substantially augmented in obese humans, which may contribute considerably to elevated levels of circulating AGT. Adipose tissue-specific regulation of AGT provides a novel insight into the clinical implications of adipose tissue RAS in human obesity. (Keyword) Adipocytes / Adipose Tissue / Adult / Angiotensinogen / Animals / Aorta / Cell Enlargement / Female / Gene Expression Regulation / Humans / Kidney / Liver / Male / Mice / Mice, Inbred C57BL / Mice, Obese / Middle Aged / Nutritional Status / Obesity / RNA, Messenger / Renin (Link to Publication Site) ● Publication site (DOI): 10.1038/ajh.2009.263 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20057360 ● Search Scopus @ Elsevier (PMID): 20057360 ● Search Scopus @ Elsevier (DOI): 10.1038/ajh.2009.263 (DOI: 10.1038/ajh.2009.263, PubMed: 20057360)
68.	Chung Thi Kim Le, Toshio Hosaka, Yoshida Masaki, Nagakatsu Harada, Hiroshi Sakaue, Tohru Sakai and Yutaka Nakaya : Exendin-4, a GLP-1 receptor agonist, directly induces adiponectin expression through protein kinase A pathway and prevents inflammatory adipokine expression., Biochemical and Biophysical Research Communications, Vol.390, No.3, 613-618, 2009. (Summary) Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor (GLP-1R) agonist that has been used as a drug injected subcutaneously for treatment of type 2 diabetes. Many studies have revealed molecular targets of Ex-4, but its influence on adipokines has not been determined. Our study showed that Ex-4 induced secretion of adiponectin into the culture medium of 3T3-L1 adipocytes. This effect of Ex-4 is due to increased adiponectin mRNA level through the GLP-1R. Both forskolin and 3-isobutyl-1-methylxanthine (IBMX), which may finally elevate cyclic adenosine monophosphate (cAMP) concentration, prevented the induction of adiponectin expression by Ex-4. Moreover, H89, a protein kinase A inhibitor, blocked the effect of Ex-4 on adiponectin. On the other hand, Ex-4 decreased the mRNA levels of inflammatory adipokines. The results indicate that Ex-4 directly promotes adiponectin secretion via the protein kinase A pathway in 3T3-L1 adipocytes and may ameliorate insulin resistance. (Keyword) 1-Methyl-3-isobutylxanthine / 3T3-L1 Cells / Adipocytes / Adipokines / Adiponectin / Animals / Cyclic AMP-Dependent Protein Kinases / Forskolin / Glucagon-Like Peptide 1 / Inflammation / insulin resistance / Isoquinolines / Mice / Peptides / Phosphodiesterase Inhibitors / Protein Kinase Inhibitors / RNA, Messenger / Receptors, Glucagon / Sulfonamides / Venoms (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2009.10.015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19850014 ● Search Scopus @ Elsevier (PMID): 19850014 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2009.10.015 (DOI: 10.1016/j.bbrc.2009.10.015, PubMed: 19850014)

Academic Paper (Unrefereed Paper):

1.	Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shinichiro Yamada, Hiroki Teraoku, Sonoko Yasui-Yamada, Maki Nishi, Hiroshi Sakaue, Motomu Kamada, Tetsuya Matsuura and Mitsuo Shimada : Preoperative Weight Loss Program for Hepatocellular Carcinoma Patients with High Body Mass Index in Hepatectomy., World journal of surgery, Vol.47, No.12, 3348-3355, 2023. (Summary) This study aimed to investigate the usefulness of a weight-loss program (WLP) in patients with a high body mass index (BMI) prior to liver resection (Hx) for hepatocellular carcinoma (HCC). Among 445 patients with HCC who underwent initial Hx between 2000 and 2020, 19 with a high BMI (≥25.0) were enrolled in our WLP since 2014. For calorie restriction, the amount of energy consumed was calculated as the standard body weight (SBW) kg × 20-25 kcal/day. Protein mass was calculated as SBW kg × 1.0-1.2 g/day to maintain skeletal muscle mass. Patients also performed both aerobic and resistance exercises. The before-and-after changes were compared, and the effect of WLP on the short- and long-term results was investigated. The average length of WLP was 21 days, and weight loss was successfully achieved in all patients. Body fat mass was reduced during the program, while skeletal muscle mass was maintained. WLP led to improvements in liver function and fibrotic markers, without tumor progression. There were no postoperative complications (≥Clavien-Dindo [CD] III). A retrospective comparison between with and without WLP using propensity score-matching analysis revealed that WLP group showed better NLR value, however, there were no significant differences in both short and long-term outcomes after Hx based on participation in the WLP. WLP with multidisciplinary intervention improved immune-nutrition status and liver function of obese patients. WLP had not affected both short and long-term outcomes after Hx. (Keyword) Humans / Carcinoma, Hepatocellular / Hepatectomy / Liver Neoplasms / Body Mass Index / Weight Reduction Programs / Retrospective Studies / Propensity Score / Treatment Outcome / Laparoscopy (Link to Publication Site) ● Publication site (DOI): 10.1007/s00268-023-07220-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37840060 ● Search Scopus @ Elsevier (PMID): 37840060 ● Search Scopus @ Elsevier (DOI): 10.1007/s00268-023-07220-0 (DOI: 10.1007/s00268-023-07220-0, PubMed: 37840060)
2.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 黒井俊哉, 植木歩夢, Rie Tsutsumi, Hiroshi Sakaue, 小瀧歩 and 工藤千秋 : 認知症超早期発見チェックシート(Q-ESD)と老研式活動能力指標(TMIG-IC)との相関性の検討, The Journal of Japan Society for Early Stage of Dementia, Vol.13, No.1, 42-48, 2020. (Summary) 目的:急速な高齢化において認知症の早期発見・早期予防が重要であるが，プレクリニカル期における簡易的に検出可能なスクリーニング方法は開発されていない．今回，我々は，認知機能低下と関係の深い日常生活の変化を捉えるべく，認知症の超早期段階における発見チェックシート;The Questionnaires for Earlier Stage of Dementia(Q-ESD)を開発した．認知症と診断されていない高齢者を対象としてQ-ESDを実施し，その有用性に関して老研式活動能力指標との関連性を比較・検討した．対象と方法:全国13施設において，認知症簡易スクリーニング法TOP-Qスコアが1点以下の認知機能低下を認めない高齢者に対し，導入時と4ヵ月後にQ-ESDと老研式活動能力指標の調査をした．結果:対象者134名(男/女=25/109)の平均年齢は75.2±12.0歳，平均Q-ESDスコアは25.0±7.0点であった．Q-ESDと老研式活動能力指標の合計スコアに負の相関(P<0.05)がみられた．Q-ESDの改善・維持群，悪化群では初回調査時の手段的，知的，社会的ADLが有意に低値であった(p<0.05)．結論:Q-ESDは生活機能の低下を早期に検出し，Q-ESDのスコアの高値は将来の認知症発症の予備軍となり得る可能性が示唆された．(著者抄録) (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / *認知症(診断) 早期診断チェックリスト Mini-Mental State 老研式活動能力指標ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523669556040598272 (CiNii: 1523669556040598272)

Review, Commentary:

1.	Hitoshi Shono, Rie Tsutsumi, Chisa Fujimoto, Masakazu Goda, Ryo Kanamura, Hiroki Ohnishi, Gou Satou, Yoshiaki Kitamura, Koji Abe, Koichi Tamura, Hiroshi Sakaue and Noriaki Takeda : Chemotherapy-Induced Taste Impairment in Patients with Head and Neck Cancer : Molecular Mechanisms and Dietary Prevention, Practica Oto-Rhino-Laryngologica. Suppl., No.158, 138-141, Feb. 2022. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390855035389806208 (CiNii: 1390855035389806208)
2.	Tsukasa Takaoka, Aki Endo, Kazunori Matsuda, 上田千鶴, 猿倉薫子, Rie Tsutsumi, Hiroshi Sakaue, Tohru Sakai, Shigeru Yamamoto and Noriaki Takeda : A Novel Method of Assessment of the Zinc Nutrition Status and Zinc Deficiency-Induced Taste Impairment, Practica Oto-Rhino-Laryngologica. Suppl., No.158, 133-137, Feb. 2022. (Link to Publication Site) ● Publication site (DOI): 10.5631/jibirinsuppl.158.133 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390573560394202496 ● Search Scopus @ Elsevier (DOI): 10.5631/jibirinsuppl.158.133 (DOI: 10.5631/jibirinsuppl.158.133, CiNii: 1390573560394202496)
3.	Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : 【脂肪細胞・アディポサイトカインと糖尿病】脂肪細胞と糖尿病褐色脂肪細胞と糖尿病, 月刊糖尿病, Vol.14, No.1, 28-34, Jan. 2022.
4.	Masataka Sata and Hiroshi Sakaue : 特集生活習慣病を克服して,健康寿命を延伸するために【巻頭言】, Shikoku Acta Medica, Vol.77, No.5,6, 173, Dec. 2021. (Tokushima University Institutional Repository) ● Metadata: 117125 (Tokushima University Institutional Repository: 117125)
5.	Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : 脂肪細胞分化に対するエピジェネティック制御機構, 実験医学増刊, Vol.39, No.5, 32-38, Mar. 2021.
6.	Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : 【個人差の理解へ向かう肥満症研究 GWAS，エピゲノム，腸内細菌，栄養学的知見から多様な病態を解明し，Precision Medicineをめざす】(第1章)代謝(エネルギー消費)の分子・細胞・個体メカニズム脂肪細胞分化に対するエピジェネティック制御機構, Experimental Medicine, Vol.39, No.5, 654-660, Mar. 2021. (Summary) 生体はヒストン修飾やDNAメチル化などのエピジェネティクスによる制御機構により染色体の局所構造を変化させて，ゲノムDNA中の膨大な情報の中から必要な遺伝子を選択して活性化・不活性化している．このエピジェネティクスによる遺伝子発現制御は幹・前駆細胞がある特定の機能をもった細胞へ分化する際にも重要な意義をもち，分化誘導中の時系列遺伝子発現プロファイルの形成に貢献している．脂肪細胞では分化のマスターレギュレーターPPARγを中心に，その誘導や標的遺伝子の活性化にかかわるエピゲノムの変化が解明されている．(著者抄録) (Keyword) Histones Histone-Lysine N-Methyltransferase 遺伝子発現調節クロマチン DNAメチル化 CCAAT-Enhancer-Binding Protein-Beta 非翻訳RNA エピジェネティックプロセス褐色脂肪細胞 Jumonji Domain-Containing Histone Demethylases 脂肪細胞分化ベージュ脂肪細胞細胞発生 Jmjd3 Protein KDM3A Protein EHMT1 Protein ヒト
7.	原加奈子, Rie Tsutsumi, Nobuto Nakanishi, 三島優奈, 待田京香, Masashi Kuroda, Jun Oto and Hiroshi Sakaue : 重症患者における筋萎縮と尿中タイチン濃度測定の意義, Shikoku Acta Medica, Vol.76, No.5-6, 267-272, Dec. 2020. (Summary) タイチンは，骨格筋において最初に分解される蛋白質として注目されている．尿中のタイチンN末端断片濃度を測定できるELISAが開発され，筋ジストロフィー患者では健常人の数百倍のタイチンN末端断片が検出されることが報告されている．これまでに行った，重症病態における筋萎縮，筋機能低下のバイオマーカーとしての尿中タイチン濃度測定の有用性についての研究を中心に概説した． (Keyword) バイオマーカー(尿) ICU 筋萎縮症(診断,X線診断) 筋節 X線CT 病勢悪化 Connectin(尿) ヒト (Tokushima University Institutional Repository) ● Metadata: 115785 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050287363395004928 (Tokushima University Institutional Repository: 115785, CiNii: 1050287363395004928)
8.	Masashi Kuroda and Hiroshi Sakaue : Transcroptional control of thermogenic fat, Diabetology, Endocrinology & Metabolology, Vol.51, No.1, 23-27, Jul. 2020. (Keyword) thermogenesis / brown adipocytes / transcriptional control (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521699229687059584 (CiNii: 1521699229687059584)
9.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, Masashi Kuroda and Hiroshi Sakaue : 【糖・エネルギー代謝ネットワークupdate】脂肪細胞熱産生機構における転写因子による制御, Diabetology, Endocrinology & Metabolology, Vol.51, No.1, 23-27, Jul. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / DNA-Binding Proteins 転写因子肥満トランスアクチベーター熱産生 Interferon Regulatory Factors RNA-Binding Protein EWS エピジェネティックプロセス *褐色脂肪細胞脂肪細胞分化 Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-Alpha PRDM16 Protein Interferon Regulatory Factor-4 EBF1 Protein ヒト (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521699229687059584 (CiNii: 1521699229687059584)
10.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 三島優奈, Rie Tsutsumi and Hiroshi Sakaue : 代謝動態の連関による生体機能制御骨格筋と代謝調節に注目して, Diabetology, Endocrinology & Metabolology, Vol.51, No.1, 71-77, Jul. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / エネルギー代謝肝臓飢餓筋萎縮症脂肪組織身体運動絶食ホメオスタシス *骨格筋廃用症候群ヒト (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520010380610834688 (CiNii: 1520010380610834688)
11.	Masashi Kuroda and Hiroshi Sakaue : ADCY3 gene and Obesity, Endocrinology, Diabetology & Metabolism, Vol.48, No.3, 214-218, Mar. 2019. (Keyword) ADCY3 / Leptin / Melanocortin 4 receptor (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521417755406689664 (CiNii: 1521417755406689664)
12.	Masashi Kuroda and Hiroshi Sakaue : Adipocyte Death and Chronic Inflammation in Obesity, The Journal of Medical Investigation : JMI, Vol.64, No.3,4, 193-196, Aug. 2017. (Summary) Cell death is closely linked to many diseases including cancer, neurodegenerative diseases, autoimmune diseases, and metabolic disorders. Increased adipocyte death has been reported during the development of obesity. Adipocyte death may be caused by excessive stress during obesity-related adipose tissue remodeling. Adipose tissue macrophages are key players in obesity-related inflammation and systemic insulin resistance. Accumulating evidence suggests that adipocyte death is involved in immune cell function and initiates inflammation through an interaction with macrophages; however, the precise mechanisms remain largely unknown. This review focuses on the contribution of dead cells (particularly dead adipocytes in adipose tissue) to the pathophysiological conditions associated with obesity. J. Med. Invest. 64: 193-196, August, 2017. (Keyword) Adipocytes / Cell Death / Chronic Disease / Humans / Inflammation / Macrophages / Obesity (Tokushima University Institutional Repository) ● Metadata: 111114 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.193 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954980 ● Search Scopus @ Elsevier (PMID): 28954980 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.193 (Tokushima University Institutional Repository: 111114, DOI: 10.2152/jmi.64.193, PubMed: 28954980)
13.	Masashi Kuroda and Hiroshi Sakaue : [Role of vitamin D and calcium in obesity and type 2 diabetes]., Clinical Calcium, Vol.26, No.3, 349-354, Mar. 2016. (Summary) Obesity, induced by unhealthy lifestyle choices, could be involved in the development of chronic diseases like type 2 diabete. Obesity is largely due to the imbalance of energy intake and expenditure, therefore we have put more emphasis on the amount of macronutrients including carbohydrates, fats and proteins as dietary therapy for obesity and related-conditions. On the other hand, several studies revealed obese or diabetic patients were more likely to have micronutrient deficiencies such as vitamins and minerals. Besides the effects on bone metabolism, vitamin D and calcium might contribute to metabolic disorder accompanied by obesity. However, it has not been concluded supplementation of these two nutrients has a benefit in obese or diabetic individuals. Further studies are needed. (Keyword) Animals / calcium / Diabetes Mellitus, Type 2 / Dietary Proteins / Energy Intake / Humans / obesity / vitamin D (Link to Publication Site) ● Publication site (DOI): 10.20837/4201603009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26923970 ● Search Scopus @ Elsevier (PMID): 26923970 ● Search Scopus @ Elsevier (DOI): 10.20837/4201603009 (DOI: 10.20837/4201603009, PubMed: 26923970)
14.	Rie Tsutsumi, Yasuo M. Tsutsumi and Hiroshi Sakaue : 救急・集中治療重症患者の栄養治療, Vol.27, No.7.8, 585-590, Aug. 2015.
15.	Hiroshi Sakaue and 田渕正樹 : 最新臨床脳卒中学(上), Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.72, No.5, 250-252, Jun. 2014.
16.	Hiroshi Sakaue, 興津理絵 and 黒田雅士 : 肥満と肥満症基礎研究の進歩脂肪細胞の肥大と増殖(, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.72, No.4, 66-70, May 2014.
17.	黒田雅士 and Hiroshi Sakaue : I. Q 6．脂肪における高血糖の急性毒性, 救急・集中治療, Vol.24, No.5-6, 545-550, Jun. 2012.
18.	Hiroshi Sakaue : 栄養学からみた糖尿病・肥満研究(1), プラクティス, Vol.28, No.6, 549-551, Nov. 2011.
19.	福田亜希子 and Hiroshi Sakaue : 飽和脂肪酸とメタボの関係は? 飽和脂肪酸を摂るとメタボになりやすいですか?(動物実験の結果を含めて), Q&Aでわかる肥満と糖尿病, Vol.10, No.6, 846-848, Nov. 2011.
20.	Hiroshi Sakaue : 栄養学からみた糖尿病・肥満研究(2), プラクティス, Vol.28, No.5, 451-453, Sep. 2011.
21.	Hiroshi Sakaue : 成因と病態生理メタボリックシンドローム発症基盤としての脂肪細胞機能異常脂肪細胞分化・増殖の制御機構とその破綻, 日本臨床, Vol.69, No.1, 206-210, Jan. 2011.
22.	Hiroshi Sakaue : 脂肪細胞の数と大きさの制御と病態生理的意義, 内分泌・糖尿病・代謝内科, Vol.31, No.6, 519-525, Dec. 2010.
23.	Hiroshi Sakaue : 脂肪細胞数の制御機構と炎症, 糖尿病の進歩, Vol.44, 196-200, Sep. 2010.
24.	Yutaka Nakaya, Nagakatsu Harada, 堤理絵 and Hiroshi Sakaue : 肝硬変に対する栄養サポートのエビデンス, 静脈経腸栄養, Vol.25, No.5, 1057-1062, 2010.

Proceeding of International Conference:

1.	Masashi Kuroda, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : Transcription factor IRF7 and energy metabolism, The 11th Scientific Meeting of the Asian Association for the Study of Diabetes., May 2019.
2.	Nishimoto Sachiko, Daiju Fukuda, Higashikuni Yasutomi, Tanaka Kimie, Hirata Yoichiro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Genetic deletion of TLR9 promotes blood flow recovery in hind limb ischemia, 19th International Vascular Biology Meeting, Nov. 2016.
3.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Toll-like Receptor 9 Plays a Pivotal Role in Angiotensin II-induced Atherosclerosis., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
4.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : The activation of toll-like receptor 9 deteriorates blood flow recovery after hind-limb ischemia., ESC Congress 2015, London, Aug. 2015.
5.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura, H. Hagita, Y. Miyatake, Hiroshi Sakaue and Takafumi Noma : Gene expression analysis of hyperactive mutant SPORTS rat, Cell Symposia:Exercise and Metabolism which takes place at NH Grand Krasnapolsky Hotel Amsterdam from 12-14 July 2015, Amsterdam, Jul. 2015.
6.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Genetic deletion of toll-like receptor 9 accelerates blood flow recovery after hindlimb ischemia., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
7.	Hiroshi Sakaue and 黒田雅士 : Role of DNA methylation for leptin gene promoter in 3T3-L1 adipocytes, Mar. 2014.
8.	Hiroshi Sakaue and 興津理恵 : Role of the new microtubule-associated protein in the development of obesity, 国際肥満学会, Mar. 2014.
9.	S Nishimoto, Daiju Fukuda, Michio Shimabukuro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Macrophage Toll-like Receptor 9 Signaling Contributes to the Development of Insulin Resistance through the Promotion of Inflammation in Adipose Tissue., American Heart Association AHA 2013, Dallas, Nov. 2013.
10.	S Nishimoto, Daiju Fukuda, Michio Shimabukuro, S Matsumoto, Masayoshi Ishida, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Genetic ablation of TLR9 improves insulin resistance through macrophage accumulation in adipose tissue., ESC Congress 2013, Amsterdam, Aug. 2013.
11.	H. Sato, Michio Shimabukuro, Y. Hirata, Hirofumi Izaki, M. Higashida, Hirotsugu Kurobe, Hiro-omi Kanayama, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Region-specific regulation of the innate immune system, NLRP3 inflammasome, in human abdominal adipose tissue., ESC Congress 2012, Munich, Aug. 2012.
12.	Yutaka Nakaya, Shimohata Takaaki, Haraguchi Sayaka, Nakao Toshiyuki, Minaguchi Jun, Sumitani Haruo, Nagakatsu Harada and Hiroshi Sakaue : Severe Catabolic State After An Overnight Fast In Patients With Chronic Renal Failure, 31stESPEN Congress, Wien, Aug. 2009.

Proceeding of Domestic Conference:

1.	Hiroshi Sakaue : エネルギー代謝に関わる末梢組織のバイオロジー白色脂肪組織のバイオロジー, 第31回日本肥満学会 2010年10月,
2.	Hiroshi Sakaue : NSTを始めるために必要な栄養管理の知識症例に基づく経腸管理の実際, 第14会日本病態栄養学会2011年1月,
3.	Sonoko Yasui-Yamada, Miyu Kubo, Yuna Izumi, Kazuhiro Nomura, Seiichiro Kamimura, Hideya Kashihara, Yu Saitou, Yoshiaki Kitamura, Mitsuo Shimada, Yasuhiro Hamada and Hiroshi Sakaue : 簡便に得られるデータから作成した四肢骨格筋量を予測する回帰式の妥当性検証, 第27回日本病態栄養学会年次学術集会, Jan. 2024.
4.	Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shin-ichiro Yamada, Hiroki Teraoku, Sonoko Yasui-Yamada, Hiroshi Sakaue, 鎌田基夢, Tetsuya Matsuura and Mitsuo Shimada : 肥満を有する肝細胞癌患者に対する術前栄養運動介入の有用性 - ERAS導入による手術成績の向上 –, 第78回日本消化器外科学会総会, Jul. 2023.
5.	Yu Saitou, Yuji Morine, Shin-ichiro Yamada, Hiroki Teraoku, Tetsuya Ikemoto, Sonoko Yasui-Yamada, Hiroshi Sakaue, 鎌田基夢, Tetsuya Matsuura and Mitsuo Shimada : 肥満を有する肝細胞癌患者に対する術前栄養運動介入の有用性-ERAS導入による手術成績の向上 –, 日本外科代謝栄養学会第60回学術集会, Jul. 2023.
6.	Yu Saitou, Yuji Morine, Shin-ichiro Yamada, Hiroki Teraoku, Tetsuya Ikemoto, Shin-ichiro Yamada, 西麻希, Hiroshi Sakaue, 鎌田基夢, Tetsuya Matsuura and Mitsuo Shimada : Preoperative weight loss program for high body mass index patients undergoing liver resection for hepatocellular carcinoma - Surgical outcomes of ERAS protocol, 第35回日本肝胆膵外科学会学術集会, Jun. 2023.
7.	Hiroki Teraoku, Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shin-ichiro Yamada, Sonoko Yasui-Yamada, 西麻希, Hiroshi Sakaue, 鎌田基夢, Tetsuya Matsuura and Mitsuo Shimada : 肝細胞癌における肥満患者への術前栄養運動介入の有用性, 第123回日本外科学会定期学術集会, Apr. 2023.
8.	Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shin-ichiro Yamada, Hiroki Teraoku, Sonoko Yasui-Yamada, 西麻希, Hiroshi Sakaue, 鎌田基夢, Tetsuya Matsuura and Mitsuo Shimada : 肥満を有する肝細胞癌患者に対する術前栄養運動介入の有用性, 第118回日本消化器病学会四国支部例会, Nov. 2022.
9.	Yu Saitou, Yuji Morine, Shin-ichiro Yamada, Hiroki Teraoku, Toshiaki Yoshimoto, 西麻希, Hiroshi Sakaue and Mitsuo Shimada : 肥満肝細胞癌患者に対する術前栄養運動介入の有用性 -ERAS導入による手術成績の向上-, 第60回日本癌治療学会学術集会, Oct. 2022.
10.	Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shin-ichiro Yamada, Hiroki Teraoku, Toshiaki Yoshimoto, 西麻希, Hiroshi Sakaue and Mitsuo Shimada : 肥満を有する肝細胞癌患者に対する術前栄養運動介入の有用性, 第77回日本消化器外科学会総会, Jul. 2022.
11.	Yu Saitou, Yuji Morine, Tetsuya Ikemoto, Shin-ichiro Yamada, Hiroki Teraoku, Masaaki Nishi, Hiroshi Sakaue and Mitsuo Shimada : Weight loss program for high body mass index patients undergoing liver resection for hepatocellular carcinoma, 第34回日本肝胆膵外科学会・学術集会, Jun. 2022.
12.	WADA Azumi, Masashi Kuroda, TAMURA Yumi, CHAMOTO Rin, TOMINAGA Rena, KOBAYASHI Kuroe, MATSUMURA Erika, Miyuki Takishita, MEI Fujita, Rie Tsutsumi and Hiroshi Sakaue : 脂肪組織由来MFG-E8はNASHでの肝慢性炎症・線維化を促進する, 第42回日本肥満学会, Mar. 2022.
13.	Masashi Kuroda, TOMINAGA Rena, TAMURA Yumi, CHAMOTO Rin, MATSUMURA Erika, KOBAYASHI Kuroe, WADA Azumi, Miyuki Takishita, MEI Fujita, Tetsuya Shiuchi, Rie Tsutsumi and Hiroshi Sakaue : エネルギー代謝調節機構における転写因子IRF7生理的意義の検討, 第25回アディポサイエンス・シンポジウム, Feb. 2022.
14.	Masashi Kuroda, CHAMOTO Rin, TAMURA Yumi, TOMINAGA Rena, KOBAYASHI Kuroe, MATSUMURA Erika, WADA Azumi, Miyuki Takishita, MEI Fujita, Rie Tsutsumi and Hiroshi Sakaue : DNAメチル化による熱産生関連遺伝子制御機構の検討, 第 54 回日本栄養•食糧学会中国•四国支部大会, Oct. 2021.
15.	WADA Azumi, CHAMOTO Rin, TAMURA Yumi, TOMINAGA Rena, KOBAYASHI Kuroe, MATSUMURA Erika, Miyuki Takishita, MEI Fujita, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : NASH病態形成における脂肪組織由来分泌タンパク質MFG-E8の関与, 第263回徳島医学会, Aug. 2021.
16.	Masashi Kuroda, CHAMOTO Rin, TOMINAGA Rena, TAMURA Yumi, MATSUMURA Erika, Miki Ogawa, Rie Tsutsumi and Hiroshi Sakaue : DNAメチル化による脂肪細胞機能制御についての検討, 第64回日本糖尿病学会年次学術集会, May 2021.
17.	出葉祥恵, 山下果穂, 竹治香菜, 山崎幸, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : ストレプトゾトシン抵抗性ラットに認められた消化管・膵臓連関, Journal of the The Japan Diabetes Society, Vol.64, No.Suppl.1, III-94-6, May 2021.
18.	Mai Kanai, 長井輝幸, Itsuro Endo, 大西幸代, 原倫世, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, 瀬部真由, Hiroshi Sakaue, Seiji Fukumoto, 松本俊夫 and 安倍正博 : TAK1阻害による炎症性サイトカイン誘導性骨格筋萎縮の改善, Folia endocrinologica Japonica, Vol.97, No.1, 365, Apr. 2021. (Keyword) cytokinesis / 筋萎縮症(遺伝学,病理学,実験的) / 骨格筋(病理学) / 腫瘍壊死因子アルファ / 核内受容体NR2C2(拮抗物質・阻害物質) / マウス / animal
19.	MISHIMA Yuna, Rie Tsutsumi, Tamaki Otani, Kanako Hara, Saori Fujimoto, Masashi Kuroda and Hiroshi Sakaue : PET/CTを用いたマウス骨格筋インスリン抵抗性の評価, 第41回日本肥満学会, Mar. 2021.
20.	岡松優子, Masashi Kuroda, Rie Tsutsumi, 坪田あゆみ, 斉藤昌之, 木村和弘 and Hiroshi Sakaue : マウス褐色脂肪組織において寒冷刺激により誘導されるUCP1依存的および非依存的代謝変化, 第41回日本肥満学会, Mar. 2021.
21.	MATSUMURA Erika, Masashi Kuroda, TOMINAGA Rena, TAMURA Yumi, CHAMOTO Rin, KOBAYASHI Kuroe, WADA Azumi, Miyuki Takishita, MEI Fujita, Tetsuya Shiuchi, Rie Tsutsumi and Hiroshi Sakaue : 転写因子IRF7によるエネルギー代謝調節機構の解明, 第42回日本肥満学会, Mar. 2021.
22.	原加奈子, Rie Tsutsumi, 三島優奈, 待田京香, Hiroshi Sakaue, Nobuto Nakanishi and Jun Oto : 重症患者における筋萎縮と尿中タイチン濃度に関する検討, Shikoku Acta Medica, Vol.76, No.5-6, 341, Dec. 2020. (Keyword) *筋萎縮症(診断) / 病勢悪化 / Connectin(尿) / ヒト
23.	Rie Tsutsumi, Hiroshi Sakaue, 敷島康普 and Hiroyuki Miura : スダチ果皮エキス末の継続摂取が内臓脂肪に与える影響についてのランダム化二重盲検介入試験, Shikoku Acta Medica, Vol.76, No.5-6, 341-342, Dec. 2020. (Keyword) 植物抽出物(治療的利用) / 二重盲検法 / ミカン属(治療的利用) / ランダム化比較試験 / メタボリックシンドローム(食事療法,X線診断) / 腹腔内脂肪(X線診断) / ヒト / 男 / 女
24.	三島優奈, Rie Tsutsumi, Masashi Kuroda, Hiroshi Sakaue and Tamaki Otani : PET/CTを用いたマウス骨格筋インスリン抵抗性の評価, Shikoku Acta Medica, Vol.76, No.5-6, 342, Dec. 2020. (Keyword) インスリン抵抗性(実験的) 骨格筋(X線診断,放射性核種診断) *PET-CT検査マウス動物
25.	Rie Tsutsumi, 福永佳容子, 阿久根愛実, 植木歩夢, 黒井俊哉, 藤田智子, 小瀧歩, 工藤千秋 and Hiroshi Sakaue : 認知症患者の栄養管理の問題点と工夫早期認知機能低下高齢者に認められる食の変化, Online Journal of JSPEN, Vol.2, No.Suppl.1, 153, Nov. 2020. (Keyword) 食行動認知機能低下食物摂取頻度調査ヒト中年(45~64) 高齢者(65~79) 高齢者(80~)
26.	Rie Tsutsumi, 山本智子, 橘高久未子, Nobuto Nakanishi and Hiroshi Sakaue : 重症患者の栄養代謝病態と栄養療法の実際重症病態における糖・アミノ酸代謝動態の解明, Online Journal of JSPEN, Vol.2, No.Suppl.1, 187, Nov. 2020. (Keyword) Amino Acids ICU 敗血症(実験的) タンパク質代謝 *糖代謝メタボロミクスヒトマウス動物高齢者(65~79) 男女
27.	別府香名, Rie Tsutsumi, 瀬部真由 and Hiroshi Sakaue : 食道がん・頭頸部がん患者における安静時エネルギー消費量と食事摂取量および体組成の関係性, Online Journal of JSPEN, Vol.2, No.Suppl.1, 252, Nov. 2020. (Keyword) 基礎代謝食行動食道腫瘍頭頸部腫瘍 *身体組成ヒト中年(45~64) 高齢者(65~79)
28.	瀬部真由, Rie Tsutsumi, 瀬野浦聖佳, Jun Kishi, Masashi Kuroda, 木下成三, Yutaka Nakaya, Yasuo Tsutsumi, Yasuhiko Nishioka and Hiroshi Sakaue : 脂質の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, Online Journal of JSPEN, Vol.2, No.Suppl.1, 824, Nov. 2020. (Keyword) 関節リウマチ(病因,合併症,実験的) 食品中の脂肪(毒性・副作用) 病勢悪化筋肉減少症(病因,合併症,実験的) *高脂肪食(有害作用) ヒトマウス動物中年(45~64) 女
29.	Aki Endo, MATSUOKA Momoyo, Tsukasa Takaoka, Rie Tsutsumi, Hiroshi Sakaue and Noriaki Takeda : 難治性亜鉛欠乏性味覚障害患者に対するツイントース併用亜鉛補充療法の効果, 第121回日本耳鼻咽喉科学会学術講演会, Oct. 2020.
30.	Hitoshi Shiyouno, Rie Tsutsumi, Ryo Kanamura, Hiroki Ohnishi, Gou Satou, Yoshiaki Kitamura, Koji Abe, Hiroshi Sakaue and Noriaki Takeda : 食事へのグルタミン酸Na 添加が頭頸部癌患者の化学療法による舌粘膜の味覚受容体遺伝子発現に与える影響, 第121回日本耳鼻咽喉科学会学術講演会, Oct. 2020.
31.	徳里望, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 庄野仁志, 阿部亮, 大西皓貴, Gou Satou, Yoshiaki Kitamura, Koji Abe, Hiroshi Sakaue and Noriaki Takeda : 食事へのグルタミン酸Na添加が頭頸部癌患者の化学療法による舌粘膜の味覚受容体遺伝子発現に与える影響, Journal of Otolaryngology of Japa, Vol.123, No.4, 1065, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Sodium Glutamate(治療的利用,薬理学) 遺伝子発現口腔粘膜抗腫瘍剤(治療的利用,毒性・副作用) 頭頸部腫瘍(薬物療法) 味覚障害(化学的誘発,薬物療法) 味蕾舌粘膜ヒト
32.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 河相舞香, 竹治香菜, 山崎幸, 松本裕華, Rie Tsutsumi, Masashi Kuroda and Hiroshi Sakaue : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, Journal of the The Japan Diabetes Society, Vol.63, No.9, 642, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Insulin Streptozocin(毒性・副作用) 薬物抵抗性細胞保護 *インスリン分泌細胞 Ghrelin(血液) Glucagon-Like Peptide 1(血液) ラット動物
33.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 原加奈子, Rie Tsutsumi, 三島優奈, 松本裕華, Masashi Kuroda, Tamaki Otani and Hiroshi Sakaue : PET/CTを用いた代謝性疾患モデルマウス骨格筋糖取り込みの評価, Journal of the The Japan Diabetes Society, Vol.63, No.9, 649, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 高インスリン症(実験的) 疾患モデル(動物) 骨格筋(X線診断,放射性核種診断) Fluorodeoxyglucose F18(診断的利用) PET-CT検査マウス動物オス
34.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 森万理恵, 別府香名, Rie Tsutsumi, Hiroyasu Mori, Munehide Matsuhisa, Hiroshi Sakaue, 神田彩恵, Rie Tsutsumi, 三島優奈, 上嶋奈々子, 松本裕華, 原加奈子, Masashi Kuroda and Hiroshi Sakaue : ロイシンの抗動脈硬化作用の検討, Journal of the The Japan Diabetes Society, Vol.63, No.9, 657, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 血液透析糸球体濾過量腎不全-慢性(治療,合併症) 糖尿病(合併症) 味覚障害(病因) 味蕾 Leptin(血液) G-Protein-Coupled Receptors T1R Receptor ヒト / Cholesterol(血液) Leucine(治療的利用) LDL Cholesterol(血液) 動脈硬化症(薬物療法,実験的) マウス動物メス
35.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 岡本彩椰, Masashi Kuroda, 川端康代, 田村優実, 富永玲奈, Rie Tsutsumi and Hiroshi Sakaue : NASH病態形成における脂肪組織由来分泌タンパク質MFG-E8の関与, Journal of the The Japan Diabetes Society, Vol.63, No.9, 668, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Aspartate Aminotransferases(血液) 表面抗原脂肪組織糖尿病(合併症) 乳タンパク質肝線維症肝疾患-非アルコール性脂肪性(実験的,合併症) MFGE8 Protein マウス動物
36.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 瀬部真由, Rie Tsutsumi, Masashi Kuroda and Hiroshi Sakaue : 高脂肪食摂取が関節リウマチ病態に与える影響, Journal of the The Japan Diabetes Society, Vol.63, No.9, 668, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(実験的) 肥満 CD4陽性T細胞リスク評価 Interleukin-17 高脂肪食マウス動物
37.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda and Saeko Masumoto : リンゴ由来プロシアニジンの摂取が老化モデルマウスの肥満・認知機能に及ぼす影響, Journal of the The Japan Diabetes Society, Vol.63, No.9, 668, Sep. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物
38.	Rie Tsutsumi, 山本智子, Nobuto Nakanishi and Hiroshi Sakaue : 侵襲時における臓器障害連関を科学する~基礎から臨床まで~ 侵襲時における臓器連関による糖・アミノ酸代謝制御機構の解明, Journal of the Japanese Society of Intensive Care Medicine, Vol.27, No.Suppl., 277, Sep. 2020. (Keyword) Amino Acids 肝臓骨格筋糖代謝ヒトマウス動物中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
39.	中西信人, Rie Tsutsumi, 原加奈子, 山本智子, Yumiko Tsunano, Emiko Nakataki, Taiga Itagaki, 松尾雅文, Hiroshi Sakaue and Jun Oto : 侵襲時における臓器障害連関を科学する~基礎から臨床まで~ ICU入室患者における筋萎縮と尿中タイチン濃度に関する検討, Journal of the Japanese Society of Intensive Care Medicine, Vol.27, No.Suppl., 277, Sep. 2020. (Keyword) ICU 筋萎縮症(超音波診断) *Connectin(尿) ヒト中年(45~64) 高齢者(65~79) 高齢者(80~)
40.	Rie Tsutsumi, 山本智子, Nobuto Nakanishi and Hiroshi Sakaue : 重症患者に対する栄養療法の工夫と実践重症患者の栄養管理におけるBIAの意義と活用の検討, Journal of the Japanese Society of Intensive Care Medicine, Vol.27, No.Suppl., 317, Sep. 2020. (Keyword) インピーダンス身体組成 *栄養管理ヒト男女
41.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 原加奈子, Rie Tsutsumi, Nobuto Nakanishi and Hiroshi Sakaue : 【重症患者の長期予後を見据えた栄養療法と運動療法】重症病態における代謝変化とアミノ酸代謝の見解, The Japanese Journal of Surgical Metabolism and Nutrition, Vol.54, No.3, 143-146, Aug. 2020. (Summary) 熱傷や多発外傷，敗血症といった重症病態では，健常時と比較して代謝動態は著しく変化する．侵襲時での炎症性サイトカインや免疫細胞の活性化によって解糖経路の亢進やミトコンドリアの機能不全による酸化的リン酸化の抑制が生じる．このような代謝の変化によってエネルギー代謝の倹約と乳酸の過剰産生が示唆される．また，代謝動態への影響は糖代謝のみではなくアミノ酸代謝にも及ぶ．特に分岐鎖アミノ酸(BCAA)の代謝動態は重要なシグナル因子となっている可能性が考えられる．敗血症においては，骨格筋でのロイシン抵抗性が懸念されるが，一方でロイシンの投与によって骨格筋減少抑制効果があることも報告されている．重症病態において代謝機構の変化に合わせたエネルギー投与量の調整ともに，アミノ酸代謝の意義を究明する必要がある．(著者抄録) (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Amino Acids(血液) Branched-Chain Amino Acids 運動療法活性酸素筋萎縮症(予防) 代謝栄養管理ヒト
42.	Rie Tsutsumi, 敷島康普, Hiroyuki Miura and Hiroshi Sakaue : スダチ果皮エキスによるメタボリックシンドローム予防効果のランダム化二重盲検試験, Journal of the The Japan Diabetes Society, Vol.63, No.Suppl.1, S-180, Aug. 2020. (Keyword) 植物抽出物(治療的利用) 二重盲検法ミカン属(治療的利用) 治療成績ランダム化比較試験 *メタボリックシンドローム(予防,薬物療法,予後) ヒト男女
43.	瀬部真由, Rie Tsutsumi, 瀬野浦聖佳, Jun Kishi, Masashi Kuroda, 木下成三, Yutaka Nakaya, Yasuo Tsutsumi, Yasuhiko Nishioka and Hiroshi Sakaue : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, Journal of the The Japan Diabetes Society, Vol.63, No.Suppl.1, S-329, Aug. 2020. (Keyword) 関節リウマチ(食事療法) 脂肪酸(毒性・副作用) 骨格筋病勢悪化 *筋肉減少症(化学的誘発) 筋量ヒト女
44.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, 瀬部真由, 岸潤, 木下成三, 西岡安彦 and 阪上浩 : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, 日本臨床分子医学会学術総会プログラム・抄録集, No.9, 75, Apr. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(病因) 脂肪酸骨格筋病勢悪化 *筋肉減少症(病因) 高脂肪食ヒトマウス動物女
45.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 瀬部真由, Rie Tsutsumi, 瀬野浦聖佳, Masashi Kuroda, Yutaka Nakaya, Hiroshi Sakaue, Jun Kishi, 木下成三, Yasuo Tsutsumi and Yasuhiko Nishioka : 飽和脂肪酸の過剰摂取は関節リウマチを増悪させ骨格筋量の減少を引き起こす, Shikoku Acta Medica, Vol.76, No.1-2, 120-121, Apr. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 栄養評価関節リウマチ(実験的,合併症,診断) 脂肪酸(薬理学) *骨格筋身体組成筋肉減少症(実験的,合併症,診断) ヒトマウス動物中年(45~64) 女
46.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, Eiji Takeda, 佐藤美智子, 隅田奈美, 久米寛子, 大前博司, 森下照大, 川浦昭彦, Takafumi Katayama, Rie Tsutsumi, Hiroshi Sakaue and Yutaka Taketani : 骨格筋肉量，機能，栄養素吸収におよぼす1日1000IUのビタミンD摂取効果, Vitamins, Vol.94, No.4, 277, Apr. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Hydroxycholecalciferols(血液) Vitamin D(薬理学) 筋骨格系生理学的現象乳骨格筋身体組成生理的吸収筋量ヒト成人(19~44) 中年(45~64) 高齢者(65~79) 男女
47.	Mayu Sebe, Rie Tsutsumi, Satoka Senoura, Jun Kishi, Masashi Kuroda, 木下成三, Yutaka Nakaya, Yasuo Tsutsumi, Yasuhiko Nishioka and Hiroshi Sakaue : 飽和脂肪酸の過剰摂取は関節リウマチ病態の憎悪・骨格筋量の減少を引き起こす, 第23回日本病態栄養学会年次学術集会, Jan. 2020.
48.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 瀬部真由, Rie Tsutsumi, 瀬野浦聖佳, Jun Kishi, Masashi Kuroda, 木下成三, Yutaka Nakaya, Yasuo Tsutsumi, Yasuhiko Nishioka and Hiroshi Sakaue : 飽和脂肪酸の過剰摂取は関節リウマチ病態の増悪・骨格筋量の減少を引き起こす, The Journal of Metabolism and Clinical Nutrition, Vol.23, No.Suppl., S-1, Jan. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 関節リウマチ(化学的誘発,実験的) 危険因子脂肪酸(毒性・副作用) 骨格筋病勢悪化過栄養(化学的誘発,実験的) 筋肉減少症(化学的誘発,実験的) 筋量マウス動物
49.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 阿久根愛実, Rie Tsutsumi, 植木歩夢, 瀬部真由, 黒井俊哉, 藤田智子, 小瀧歩, 工藤千秋 and Hiroshi Sakaue : 認知機能低下と食事摂取・口腔細菌叢の関連性の検討, The Journal of Metabolism and Clinical Nutrition, Vol.23, No.Suppl., S-46, Jan. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 細菌食行動食肉食品中のタンパク質無機栄養素野菜認知機能低下(予防,診断) 消化管微生物叢 *口腔内細菌ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
50.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 三島優奈, Rie Tsutsumi, 松本裕華, 原加奈子, Tamaki Otani, 上嶋菜々子, 神田彩恵, Masashi Kuroda and Hiroshi Sakaue : 廃用性筋萎縮モデルにおける骨格筋・肝代謝動態の連関による生体機能制御, The Journal of Metabolism and Clinical Nutrition, Vol.23, No.Suppl., S-54, Jan. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 遺伝子発現エネルギー代謝筋萎縮症(実験的) 骨格筋糖代謝廃用症候群(実験的) Large Neutral Amino Acid-Transporter 1 マウス動物
51.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 橘高久未子, 山本智子, Rie Tsutsumi, Nobuto Nakanishi and Hiroshi Sakaue : 重症病態における血中遊離アミノ酸の意義, The Journal of Metabolism and Clinical Nutrition, Vol.23, No.Suppl., S-57, Jan. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Amino Acids ICU エネルギー代謝前向き研究 *メタボロミクスヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
52.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, 竹治香菜, 山崎幸, 河相舞香, 松本裕華, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, The Journal of Metabolism and Clinical Nutrition, Vol.23, No.Suppl., S-57, Jan. 2020. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / Streptozocin(毒性・副作用) 糖尿病(実験的) 薬物抵抗性インスリン分泌細胞 Glucagon-Like Peptide 1(血液) ラット動物
53.	Kana Takeji, Yuki Yamasaki, Maika Kawai, Yuka Matsumoto, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : ストレプドゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 第23回日本病態栄養学会年次学術集会, Jan. 2020.
54.	MISHIMA Yuna, Rie Tsutsumi, Yuka Matsumoto, Kanako Hara, Tamaki Otani, Nanako Ueshima, 神田彩恵, Masashi Kuroda and Hiroshi Sakaue : 廃用性筋萎縮モデルにおける骨格筋・艦隊者動態の連関による生体機能制御, 第23回日本病態栄養学会年次学術集会, Jan. 2020.
55.	森万理江, Kana Beppu, Rie Tsutsumi, Hiroyasu Mori, Munehide Matsuhisa and Hiroshi Sakaue : 糖尿病および透析患者における味覚障害と舌味覚受容体発言の関連について, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
56.	Rie Tsutsumi, Mayu Sebe, Jun Kishi, Satoka Senoura, Masashi Kuroda, Yasuhiko Nishioka and Hiroshi Sakaue : 飽和脂肪酸はインスリン抵抗性誘導を介して慢性関節リウマチを増悪させる, 第40回日本肥満学会, Nov. 2019.
57.	Yasuyo Kawabata, Masashi Kuroda, Saya Okamoto, TAMURA Yumi, TOMINAGA Rena, Rie Tsutsumi and Hiroshi Sakaue : エネルギー代謝調節機構における転写因子IRF7の役割, 第40回日本肥満学会, Nov. 2019.
58.	Kana Takeji, Yuki Yamasaki, Maika Kawai, Yuka Matsumoto, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue : ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索, 第40回日本肥満学会, Nov. 2019.
59.	Noriaki Takeda, 高岡司, Rie Tsutsumi and Hiroshi Sakaue : 難治性亜鉛欠乏性味覚障害患者に対するツイントース併用亜鉛補充療法の効果, 第32回日本口腔咽頭科学会, Sep. 2019.
60.	Hitoshi Shiyouno, Rie Tsutsumi, Hiroshi Sakaue, Masakazu Goda and Noriaki Takeda : シスプラチンによる舌粘膜の味覚受容体発現低下とグルコサミン酸Naの食事への添加の効果, 第32回日本口腔咽頭科学会, Sep. 2019.
61.	Yasuyo Kawabata, Masashi Kuroda, Saya Okamoto, TAMURA Yumi, TOMINAGA Rena, Rie Tsutsumi and Hiroshi Sakaue : エネルギー代謝調節機構における転写因子IRF7の役割, 第24回アディポサイエンス・シンポジウム, Aug. 2019.
62.	徳里望, Hiroshi Sakaue, Rie Tsutsumi, Masashi Kuroda, Saeko Masumoto, Hiroshi Sakaue and Rie Tsutsumi : 肥満をもう一度考える:新たな肥満症から治療まで肥満から読み解く高齢者栄養の問題点と管理の実際, 日本抗加齢医学会総会プログラム・抄録集, No.9, 137, Jun. 2019. (Keyword) Catechin 肥満(実験的) Biflavonoids Proanthocyanidins 認知機能低下(実験的) 消化管微生物叢 Procyanidin マウス動物 / 危険因子肥満(合併症,治療) 栄養管理筋肉減少症(合併症,治療) 認知機能低下(病因,治療) フレイル(病因,治療) ヒト高齢者(65~79) 高齢者(80~)
63.	Misuzu Yamada, Akio Kuroda, Rie Tsutsumi, 冨永ゆかり, Hiroshi Sakaue and Munehide Matsuhisa : 循環血中遊離DNAを標的とした血管内皮細胞傷害の検出, 第62回日本糖尿病学会年次学術集会, May 2019.
64.	Yasuyo Kawabata, Masashi Kuroda, Naho Ugawa, Etsuko Ishikawa, Saya Okamoto, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : 肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討, 第62回日本糖尿病学会, May 2019.
65.	MISHIMA Yuna, Rie Tsutsumi, Yumiko Miyatake, Naoya Suemasa, Tamaki Otani, Naoko Kodama, Yohsuke Tamba, Masashi Kuroda, Saeko Masumoto and Hiroshi Sakaue : PET/CTを用いた代謝異常時の骨格筋における糖取り込みの測定, 第62回日本糖尿病学会, May 2019.
66.	Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Saya Okamoto, Yasuyo Kawabata, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : 脂肪組織慢性炎症及びNASH病態形成における分泌タンパク質MFG-E8の関与, 第62回日本糖尿病学会, May 2019.
67.	Kana Beppu, Rie Tsutsumi, Hiroyasu Mori, 平野春美, 土田健司, Munehide Matsuhisa, Noriaki Takeda and Hiroshi Sakaue : 透析患者における味覚障害と味覚受容体T1R3遺伝子の発現の関連, 第258回徳島医学会学術集会ポスターセッション, Feb. 2019.
68.	Rie Tsutsumi, 山本智子, Nobuto Nakanishi and Hiroshi Sakaue : 敗血症における代謝破綻と血中遊離アミノ酸の意義, Journal of the Japanese Society of Intensive Care Medicine, Vol.26, No.Suppl., [O75-1], Feb. 2019.
69.	Waka Sasaki, Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Yasuyo Kawabata, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : 脱メチル化3T3-L1脂肪細胞のインスリン感受性調節因子の探索, 第39回日本肥満学会, Oct. 2018.
70.	Yasuyo Kawabata, Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : 肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討, 第39回日本肥満学会, Oct. 2018.
71.	Masashi Kuroda and Hiroshi Sakaue : 肥満病態形成におけるIRF7の二つの役割, 第39回日本肥満学会, Oct. 2018.
72.	Masashi Kuroda, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue : エネルギー代謝における転写因子IRF7の役割, 第23回アディポサイエンス・シンポジウム, Aug. 2018.
73.	Naho Ugawa, Masashi Kuroda, Etsuko Ishikawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 肥大化脂肪細胞における転写因子 IRF7 の同定と機能解析, 第61回日本糖尿病学会, May 2018.
74.	Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与, 第61回日本糖尿病学会, May 2018.
75.	Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : Adipose tissue-derived protein, MFG-E8, regulates chronic inflammation and obesity-related liver disease, 第91回日本内分泌学会, Apr. 2018.
76.	井内茉莉奈, Rie Tsutsumi, Nobuto Nakanishi, 山本智子, 田中志歩, Jun Oto, Emiko Nakataki, Mutsuo Onodera, Hiroshi Sakaue and Masaji Nishimura : 重症患者におけるエネルギー代謝動態の解析．, 第45回日本集中治療医学会学術集会, Feb. 2018.
77.	Mami Ohishi, Hiroyasu Mori, 鈴木麗子, 明比祐子, Akio Kuroda, Motoyuki Tamaki, Satoshi Taniguchi, Masashi Ishizu, Hiroshi Sakaue and Munehide Matsuhisa : 急速進行性糖尿病腎症に関連するリスク因子の検討, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
78.	Rie Tsutsumi, Jiro Takeo, Masahiro Bando, Mayu Sebe, Yuki Yamasaki, Yohsuke Tamba, Yuko Miyahara, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada and Hiroshi Sakaue : 魚油由来長鎖モノエン脂肪酸の上腕動脈内皮機能に与える効果の検討, 第38回日本肥満学会, Oct. 2017.
79.	Rumi Onoyama, Masashi Kuroda, Misa Nishiguchi, Naho Ugawa, Etsuko Ishikawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 転写制御領域解析システムを用いた3T3-L1脂肪細胞のインスリン感受性調節因子の探索, 第38回日本肥満学会, Oct. 2017.
80.	Etsuko Ishikawa, Masashi Kuroda, Misa Nishiguchi, Rumi Onoyama, Naho Ugawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与, 第38回日本肥満学会, Oct. 2017.
81.	Masashi Kuroda, Misa Nishiguchi, Rumi Onoyama, Naho Ugawa, Etsuko Ishikawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 脂肪細胞における転写因子IRF7の同定及び機能解析, 第22回アディポサイエンス・シンポジウム, Aug. 2017.
82.	Misa Nishiguchi, Masashi Kuroda, Rumi Onoyama, Naho Ugawa, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 肥大化脂肪細胞における転写因子IRF7の同定と機能解析, 第60回日本糖尿病学会年次学術集会, May 2017.
83.	Rumi Onoyama, Masashi Kuroda, Misa Nisiguchi, Naho Ugawa, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 3T3-L1脂肪細胞のインスリン感受性に対するDNAメチル化の制御機構, 第60回日本糖尿病学会年次学術集会, May 2017.
84.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者における血清IGF-1とサルコペニア罹患との関連, 第60回日本糖尿病学会年次学術集会, May 2017.
85.	Masashi Kuroda, Misa Nishiguchi, Rumi Onoyama, Naho Ugawa, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue : 新規肥満関連転写因子IRF7によるMCP-1発現制御機構の解析, 第90回日本内分泌学会学術集会, Apr. 2017.
86.	井内茉莉奈, Rie Tsutsumi, Nobuto Nakanishi, Jun Oto, Emiko Nakataki, Mutsuo Onodera, Hiroshi Sakaue and Masaji Nishimura : 重症患者における栄養投与開始時期と体組成変化の関連性の検討．, 第44回日本集中治療医学会学術集会, Mar. 2017.
87.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1がサルコペニア羅患に及ぼす影響, 第20回日本病態栄養学会年次学術集会, Jan. 2017.
88.	Yohsuke Tamba, Jiro Takeo, Masahiro Bando, Mayu Sebe, Yuki Yamasaki, Daiju Fukuda, Yuko Miyahara, Yumiko Miyatake, Naoya Suemasa, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Rie Tsutsumi, Masataka Sata and Hiroshi Sakaue : 魚油由来長鎖モノエン脂肪酸は抗動脈硬化作用を有する, 第21回病態栄養学会年次学術集会, Jan. 2017.
89.	高橋梨恵, Licht Miyamoto, 友川剛己, 宮武由実子, Hiroshi Sakaue, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 脳内グリコーゲンによる代謝調節効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
90.	Mami Ohishi, Satoshi Taniguchi, 明比祐子, Hiroyasu Mori, Yuu Tamaki, Akio Kuroda, Motoyuki Tamaki, Michiko Araki, Hiroshi Sakaue and Munehide Matsuhisa : eGFR変化量を用いた透析導入高リスク群抽出アルゴリズムの妥当性の検討, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
91.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
92.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 第14回1型糖尿病研究会, Nov. 2016.
93.	Masahiro Bando, 竹尾仁良, Daiju Fukuda, 宮原裕子, 楊志宏, 西本幸子, 齋藤沙緒理, 川上真智子, 上吉原絢, 丹波洋介, Masataka Sata and Hiroshi Sakaue : 長鎖モノエン脂肪酸を含む魚油による抗動脈硬化作用, 第37回日本肥満学会, Oct. 2016.
94.	Michiko Araki, Hiroyasu Mori, 鈴木麗子, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Akio Kuroda, Hiroshi Sakaue and Munehide Matsuhisa : 1型糖尿病患者における血清IGF-1の低下とサルコペニア羅漢との関連, 第253回徳島医学会学術集会, Jul. 2016.
95.	Ohtuka Ryo, Nagakatsu Harada, Noriko Mizusawa, Katsuhiko Yoshimoto, Kazuchika Nishitsuji, Kazumi Takaishi, 豊中屋, Hiroshi Sakaue and Hiroshi Kitahata : GADD34のC末端領域を欠損したCHO-K1細胞の樹立, 第253回徳島医学会学術集会, Jul. 2016.
96.	Sonoko Yasui, Mayu Tanimura, Matsubara Atsumi, Rie Tsutsumi, Yoshiko Tani, Akiko Matsumura, 島田亜紀, Hiroshi Sakaue, Noriaki Takeda and Yasuhiro Hamada : 頭頸部癌化学放射線療法において治療開始時のクレアチニン身長係数が有害事象や治療中断にあたえる影響, 第31回日本静脈経腸栄養学会, Feb. 2016.
97.	井内茉莉奈, Jun Oto, Rie Tsutsumi, Mutsuo Onodera, Hiroshi Sakaue, Hideaki Imanaka and Masaji Nishimura : 重症患者における栄養予後指標としての位相角の有用性．, 第43回日本集中治療医学会学術集会, Feb. 2016.
98.	西本幸子, Daiju Fukuda, 東邦康智, 田中君枝, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : 動脈硬化におけるマクロファージTLR9の役割, 第45回日本心脈管作動物質学会, Feb. 2016.
99.	Miyu Kubo, Sonoko Yasui, Mayu Tanimura, Matsubara Atsumi, Rie Tsutsumi, Yoshiko Tani, Akiko Matsumura, 島田亜紀, Hiroshi Sakaue, Noriaki Takeda and Yasuhiro Hamada : 頭頸部癌化学放射線療法において治療開始時のクレアチニン身長係数が有害事象に与える影響, 第19回日本病態栄養学会, Jan. 2016.
100.	橋本怜, Michio Shimabukuro, Salim Masdan Hotimah, 原知也, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue and Masataka Sata : 糖尿病性血管障害におけるPAR2シグナルの関与, CVMW 2015, Dec. 2015.
101.	西本幸子, Daiju Fukuda, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : 動脈硬化発症におけるマクロファージToll-like receptor 9の役割, CVMW 2015, Dec. 2015.
102.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura, Hagita Hiroko, Miyatake Yumiko, Hiroshi Sakaue and Takafumi Noma : 運動能が亢進したSPORTSラットの遺伝子発現解析, 第38回日本分子生物学会，第88回日本生化学会合同大会, Dec. 2015.
103.	荒木迪子, Hiroyasu Mori, Hisami Okumura, 多々納浩, Motoyuki Tamaki, Akio Kuroda, Hiroshi Sakaue and Munehide Matsuhisa : 食事エネルギー密度は日本人2型糖尿病患者の肥満と関連する, 第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, Oct. 2015.
104.	Abuduli Maerjianghan, 大南博和, Hiroshi Sakaue, Tamaki Otani, 上田遥香, Eiji Takeda and Yutaka Taketani : 食事性のリンが糖代謝に及ぼす影響:PET/CT用いた解析, 第36回日本肥満学会，名古屋国際会議場，愛知県名古屋市，2015年10月2日~3日, Oct. 2015.
105.	荒木迪子, Hiroyasu Mori, Hisami Okumura, 鞍田三貴, 福尾惠介, Motoyuki Tamaki, Akio Kuroda, Hiroshi Sakaue and Munehide Matsuhisa : 低エネルギー密度食が2型糖尿病患者の食行動や代謝改善に与える効果の検討, 第251回徳島医学会学術集会ポスター, Aug. 2015.
106.	Michio Shimabukuro, Daiju Fukuda, H Sato, S Nishimoto, T Hara, A Takashima, Y Hirata, Hirotsugu Kurobe, Shusuke Yagi, Takeshi Soeki, Hirofumi Izaki, Hiroshi Sakaue, Tetsuya Kitagawa, Hiro-omi Kanayama and Masataka Sata : Depot- and Gender-Specific Regulation of the Innate Immune System in Adipose Tissues: A Study from Human Biopsy Samples., 第79回日本循環器学会学術集会, Apr. 2015.
107.	Bingzi Dong, Itsuro Endo, Takeshi Kondo, 大西幸代, Hiroshi Sakaue, 相澤慎一, Masahiro Abe and Toshio Matsumoto : Interleukin-11は脂肪細胞分化を抑制する, 第88回日本内分泌学会, Apr. 2015.
108.	足立知咲, 谷佳子, 山田静恵, 西麻希, Sonoko Yasui, 菊井聡子, 橋本脩平, 長尾紀子, 秋山真敏, 大町はる佳, Akiko Matsumura, Hiroshi Sakaue and Yasuhiro Hamada : 神経性食欲不振症患者の体重増加とエネルギー必要量との関係, 第18回日本病態栄養学会, Jan. 2015.
109.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Sachiko Matsumoto, Hiroshi Sakaue, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata : MicroRNA-100 Regulates Adipocytokine Expression in Subcutaneous and Visceral Adipose Tissue: An Observation from Human Biopsy Study., 第77回日本循環器学会学術集会, Mar. 2013.
110.	Hiroshi Sakaue, 福田亜希子, 阪上浩, 黒田雅士 and Yutaka Nakaya : 培養脂肪細胞でのレプチン発現はDNA脱メチル化と転写因子による活性化の2つのステップで制御されている, 日本栄養・食糧学会大会講演要旨集, Vol.66, 185, May 2012.
111.	二見明香里, Hiroshi Sakaue, Nagakatsu Harada, Tetsuya Shiuchi and Yutaka Nakaya : 中枢神経系におけるグレリンの摂食と運動調節経路の解析, Journal of the The Japan Diabetes Society, Vol.55, No.Suppl.1, S-300, May 2012.
112.	野村和弘, 細岡哲也, Hiroshi Sakaue, 春日雅人 and 小川渉 : PGC1, 糖尿病(, Vol.55, No.Suppl.1, S-303, May 2012.
113.	野村和弘, 細岡哲也, 佐々木努, 北村忠弘, Hiroshi Sakaue, 春日雅人 and 小川渉 : PGC1α新規スプライシングバリアントのエネルギー代謝制御における機能の検討, 日本臨床分子医学会学術総会プログラム・抄録集, 73, Apr. 2012. (Keyword) transcription factor
114.	富永彩子, Hiroshi Sakaue, 福田亜希子, 黒田雅士, Nagakatsu Harada and Yutaka Nakaya : 3T3-L1培養脂肪細胞でのレプチン発現はDNA脱メチル化と転写因子誘導の2つのステップで制御されている, 第32回日本肥満学会, Sep. 2011.
115.	谷口康子, Hiroshi Sakaue, 戸田聡美, Uuganbayar Bold, 二見明香理, 佐藤蕗子, Nagakatsu Harada and Yutaka Nakaya : アディポネクチンの自発運動制御作用の検討, 第32回日本肥満学会, Sep. 2011.
116.	永礼智基, Hiroshi Sakaue and 春日雅人 : 脂肪細胞における転写因子KLF15の過剰発現はSCD1発現を抑制し，インスリン分泌を増加させる, 肥満研究, Vol.17, No.Suppl, 140, Sep. 2011.
117.	中川忠彦, Nagakatsu Harada, 吉田将紀, 宮本愛子, 川西由希子, Hiroshi Sakaue and Yutaka Nakaya : 脂質合成律速酵素GPAT2の膜トポロジー解析, 第32回日本肥満学会, Sep. 2011.
118.	富永彩子, Hiroshi Sakaue, 福田亜希子, 黒田雅士, Nagakatsu Harada and Yutaka Nakaya : 3T3-L1培養脂肪細胞でのレプチン発現はDNAメチル化と転写因子による活性化の2つのステップで制御されている, 第16回アディポサイエンス研究会シンポジウム, Aug. 2011.
119.	富永彩子, Hiroshi Sakaue, 福田亜希子, 黒田雅士, Nagakatsu Harada and Yutaka Nakaya : 3T3-L1培養脂肪細胞でのレプチン発現はDNAメチル化と転写因子による活性化の2つのステップで制御されている, 第16回アディポサイエンス研究会シンポジウム, Aug. 2011.
120.	富永彩子, Hiroshi Sakaue, 福田亜希子, Nagakatsu Harada and 中屋豊 : Journal of the The Japan Diabetes Society, Vol.54, No.Sippl.1, S-130, Apr. 2011.
121.	谷口康子, Hiroshi Sakaue, Nagakatsu Harada and Yutaka Nakaya : 中枢神経系におけるアディポネクチンの自発運動制御作用の検討, Journal of the The Japan Diabetes Society, Vol.54, No.Suppl.1, S-257, Apr. 2011.
122.	片山恵梨香, 山田静恵, Akiko Matsumura, 宇野和美, 堤理絵, Toshio Hosaka, Hiroshi Sakaue, Naomi Kameoka, Tetsuro Ohmori and Yutaka Nakaya : 外来で著明な低リン血症を示した神経性無食欲症の一例, 第14回日本病態栄養学会, Jan. 2011.
123.	東田真由子, Akiko Matsumura, 今村有希, 宇野和美, 山田静恵, 堤理絵, Toshio Hosaka, Hiroshi Sakaue and Yutaka Nakaya : NST自身による血糖管理により褥瘡治療に効果をあげた一症例, 第14回日本病態栄養学会, Jan. 2011.
124.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya, Tetsuya Shiuchi and 箕越靖彦 : 自発運動制御におけるGhrelinの役割, 第14回日本病態栄養学会，神奈川県横浜市, Jan. 2011.
125.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya and Tetsuya Shiuchi : 自発運動制御におけるGhrelinの役割, 第31回日本肥満学会, Oct. 2010.
126.	富永彩子, 永禮智基, Hiroshi Sakaue, Nagakatsu Harada, 春日雅人 and Yutaka Nakaya : 3T3-L1脂肪細胞でのレプチン発現に対するDNAメチル化の関与, 第31回日本肥満学会, Oct. 2010.
127.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya, Tetsuya Shiuchi and 箕越靖彦 : 自発運動制御におけるGhrelinの役割, 3回日本糖尿病学会総会年次学術集会, May 2010.
128.	戸田聡美, Hiroshi Sakaue, 谷口康子, Tetsuya Shiuchi, Nagakatsu Harada, Kazuaki Mawatari and Yutaka Nakaya : 自発運動制御におけるGhrelinの役割, 第64回日本栄養・食糧学会大会, May 2010.
129.	中川忠彦, Nagakatsu Harada, 吉田将紀, 宮本愛子, 川西由希子, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : 脂質合成律速酵素グリセロール-3-リン酸アシルトランスフェラーゼ2の膜トポロジー解析, 第240回徳島医学会学術集会, Feb. 2010.
130.	中川忠彦, Nagakatsu Harada, 吉田将紀, 宮本愛子, 川西由希子, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : 脂質合成律速酵素グリセロール-3-リン酸アシルトランスフェラーゼ2の膜トポロジー解析, 第240回徳島医学会学術集会, Feb. 2010.

Et cetera, Workshop:

1.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, Reiko Suzuki, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : Advanced glycation end-products are a risk for muscle weakness in patients with type2 diabetes., American Diabetes Association 78th Scientific Sessions, Jun. 2017.
2.	Kazuaki Mawatari, 吉岡愛美子, Satomi Toda, Takamasa Ohnishi, Nagakatsu Harada, Hiroshi Sakaue and Yutaka Nakaya : 高自発走行モデル動物SPORTS ratの左心房血栓形成と発症要因の解析, 第15回徳島臨床脈管研究会, Nov. 2013.
3.	Dong Bingzi, Takeshi Kondo, Itsuro Endo, Yukiyo Ohnishi, Takashi Omatsu, Shin-ichi Yoshizawa, Hiroshi Sakaue and Toshio Matsumoto : Interleukin-11 controls bone and adipose tissue mass by regulating osteoblastic and adipogenic differentiation, 4th Bone BioScience Meeting, Jun. 2013.

Report:

1.	Yoshihiko Ueno, Yosuke Seki, Takuya YABE, Shigenobu Yonemura, Hiroshi Sakaue, Hitoshi Ikushima, Hideki Fujii, Yasuhiko Shirayama, Ken-ichi Yamada, Kazuhiko Kinoshita, Eiji Sakuradani, Ray S. Furuya and Maiko Kamioka : 令和2年度徳島大学高等教育研究センターアドミッション部門報告書, 令和2年度徳島大学高等教育研究センターアドミッション部門報告書, Mar. 2021.
2.	Yoshihiko Ueno, Yosuke Seki, keiji Ido, Yasushi Takagi, Hiroshi Sakaue, Hitoshi Ikushima, Hideki Fujii, Yasuhiko Shirayama, Hideji TANAKA, Masatake Kawada, Hideaki Nagamune, Ray S. Furuya and Maiko Kamioka : 令和元年度徳島大学高等教育研究センターアドミッション部門報告書, 令和元年度徳島大学高等教育研究センターアドミッション部門報告書, Mar. 2020.
3.	Hiroshi Sakaue : サイエンスマップ2008, 148, May 2010.

Patent:

1.	Rie Tsutsumi, Hiroshi Sakaue and Noriaki Takeda : グルタミン酸を有効成分とする担がん患者の味覚及び/又は食欲障害の改善剤, .
2.	Rie Tsutsumi and Hiroshi Sakaue : .
3.	Rie Tsutsumi and Hiroshi Sakaue : (May 2018), (Nov. 2018), 2017-101459 WO2018/216715A1 (Nov. 2018).
4.	Hiroshi Sakaue, Rie Tsutsumi, Noriaki Takeda and Rina Matsushima : グルタミン酸を有効成分とする担がん患者の味覚及び/又は食欲障害の改善剤, 2016-13808 (Jan. 2016), .

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

Research on the diagnosis and prevention of Sarcopenia (Project/Area Number: 22H03535 )
Elucidation of survival mechanism through metabolites in sepsis (Project/Area Number: 21K11724 )
Identification of novel anti-obesitic component in Citrus Awa-Suzuka. (Project/Area Number: 21K05450 )
Regulatory mechanisms of fuel utilization in brown adipose tissue thermogenesis (Project/Area Number: 21H03355 )
Basic and applied research of long-chained unsaturated fatty acid for preventing anti- arteriosclerosis (Project/Area Number: 19H04055 )
Establishment of research fundation of IRF7 on the treatment of obesity and metabolic syndrome (Project/Area Number: 16K09753 )
末梢性シグナル分子による運動制御機構の解明 (Project/Area Number: 25126718 )
Role of the microtubule-associated protein in insulin-dependent glucose uptake (Project/Area Number: 24591333 )
The investigation of the interaction between insulin sensitivity and fatty acids (Project/Area Number: 24500994 )
脂肪蓄積の分子基盤における脂肪細胞アポトーシス制御機構の解明 (Project/Area Number: 23126520 )
Research for the regulation of voluntary exercise and energy metabolism by appetite-regulating factors (Project/Area Number: 22700693 )
The role of adipocyte-specific lipid-binding protein during the development of obesity (Project/Area Number: 21591151 )
Long-term voluntary exercise improves the efficacy of cerebral angiogenesis and neurogenesis in stroke-prone genetically hypertensive rats (Project/Area Number: 20500636 )
Role of KLF15 on Energy metabolic regulation (Project/Area Number: 18590988 )
脂肪細胞の細胞周期制御機構を治療標的とした肥満症治療法の確立とその応用 (Project/Area Number: 18052012 )
The impact of cell cycle progression on the development of obesity and obesity-related metabolic disorders (Project/Area Number: 16590885 )
脂肪細胞分化を制御する自己分泌性液性因子の同定とそのシグナル伝達機構の解明 (Project/Area Number: 16046214 )
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Professor : Sakaue, Hiroshi

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