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Oxidative stress in skeletal muscle impairs mitochondrial respiration and limits exercise capacity in type 2 diabetic mice

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Title: Oxidative stress in skeletal muscle impairs mitochondrial respiration and limits exercise capacity in type 2 diabetic mice
Authors: Yokota, Takashi Browse this author →KAKEN DB
Kinugawa, Shintaro Browse this author →KAKEN DB
Hirabayashi, Kagami Browse this author
Matsushima, Shouji Browse this author →KAKEN DB
Inoue, Naoki Browse this author
Ohta, Yukihiro Browse this author
Hamaguchi, Sanae Browse this author
Sobirin, Mochamad A. Browse this author
Ono, Taisuke Browse this author
Suga, Tadashi Browse this author
Kuroda, Satoshi Browse this author →KAKEN DB
Tanaka, Shinya Browse this author →KAKEN DB
Terasaki, Fumio Browse this author →KAKEN DB
Okita, Koichi Browse this author →KAKEN DB
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: exercise intolerance
insulin resistance
mitochondrial function
oxygen uptake
Issue Date: 2009
Publisher: American Physiological Society
Journal Title: American Journal of Physiology-Heart and Circulatory Physiology
Volume: 297
Issue: 3
Start Page: H1069
End Page: H1077
Publisher DOI: 10.1152/ajpheart.00267.2009
Abstract: Insulin resistance or diabetes is associated with limited exercise capacity, which can be caused by the abnormal energy metabolism in skeletal muscle. Oxidative stress is involved in mitochondrial dysfunction in diabetes. We hypothesized that increased oxidative stress could cause mitochondrial dysfunction in skeletal muscle and make contribution to exercise intolerance in diabetes. C57/BL6J mice were fed on normal diet or high fat diet (HFD) for 8 wk to induce obesity with insulin resistance and diabetes. Treadmill tests with expired gas analysis were performed to determine the exercise capacity and whole body oxygen uptake (Vo2). The work (vertical distance × body weight) to exhaustion was reduced in the HFD mice by 36%, accompanied by a 16% decrease of peak Vo2. Mitochondrial ADP-stimulated respiration, electron transport chain complex I and III activities, and mitochondrial content in skeletal muscle were decreased in the HFD mice. Furthermore, superoxide production and NAD(P)H oxidase activity in skeletal muscle were significantly increased in the HFD mice. Intriguingly, the treatment of HFD-fed mice with apocynin [10 mmol/l; an inhibitor of NAD(P)H oxidase activation] improved exercise intolerance and mitochondrial dysfunction in skeletal muscle without affecting glucose metabolism itself. The exercise capacity and mitochondrial function in skeletal muscle were impaired in type 2 diabetes, which might be due to enhanced oxidative stress. Therapies designed to regulate oxidative stress and maintain mitochondrial function could be beneficial to improve the exercise capacity in type 2 diabetes.
Type: article
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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