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Sesamin prevents decline in exercise capacity and impairment of skeletal muscle mitochondrial function in mice with high-fat diet-induced diabetes
This item is licensed under:Creative Commons Attribution 4.0 International
Title: | Sesamin prevents decline in exercise capacity and impairment of skeletal muscle mitochondrial function in mice with high-fat diet-induced diabetes |
Authors: | Takada, Shingo Browse this author →KAKEN DB | Kinugawa, Shintaro Browse this author →KAKEN DB | Matsushima, Shouji Browse this author →KAKEN DB | Takemoto, Daisuke Browse this author | Furihata, Takaaki Browse this author →KAKEN DB | Mizushima, Wataru Browse this author | Fukushima, Arata Browse this author →KAKEN DB | Yokota, Takashi Browse this author →KAKEN DB | Ono, Yoshiko Browse this author | Shibata, Hiroshi Browse this author | Okita, Koichi Browse this author →KAKEN DB | Tsutsui, Hiroyuki Browse this author →KAKEN DB |
Issue Date: | 2015 |
Publisher: | Cambridge University Press |
Journal Title: | Experimental Physiology |
Volume: | 100 |
Issue: | 11 |
Start Page: | 1319 |
End Page: | 1330 |
Publisher DOI: | 10.1113/EP085251 |
Abstract: | We previously reported that exercise capacity and skeletal muscle mitochondrial function in diabetic mice were impaired, in association with the activation of NAD(P)H oxidase. It has been reported that sesamin inhibits NAD(P)H oxidase‐induced superoxide production. Therefore, we examined whether the antioxidant sesamin could prevent a decline in exercise capacity in mice with high‐fat diet (HFD)‐induced diabetes. C57BL/6J mice were fed a normal diet (ND) or HFD, then treated or not with sesamin (0.2%) to yield the following four groups: ND, ND+Sesamin, HFD and HFD+Sesamin (n = 10 each). After 8 weeks, body weight, fat weight, blood glucose, insulin, triglyceride, total cholesterol and fatty acid were significantly increased in HFD compared with ND mice. Sesamin prevented the increases in blood insulin and lipid levels in HFD‐fed mice, but did not affect the plasma glucose. Exercise capacity determined by treadmill tests was significantly reduced in HFD mice, but almost completely recovered in HFD+Sesamin mice. Citrate synthase activity was significantly decreased in the skeletal muscle of HFD mice, and these decreases were also inhibited by sesamin. Superoxide anion and NAD(P)H oxidase activity were significantly increased in HFD mice compared with the ND mice and were ameliorated by sesamin. Sesamin prevented the decline in exercise capacity in HFD‐induced diabetic mice via maintenance of mitochondrial function, fat oxidation and attenuation of oxidative stress in the skeletal muscle. Our data suggest that sesamin may be useful as a novel agent for the treatment of diabetes mellitus. |
Rights: | http://creativecommons.org/licenses/by/4.0/ |
Type: | article |
URI: | http://hdl.handle.net/2115/76772 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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