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Oxidative stress impairs insulin signal in skeletal muscle and causes insulin resistance in postinfarct heart failure

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Title: Oxidative stress impairs insulin signal in skeletal muscle and causes insulin resistance in postinfarct heart failure
Authors: Ohta, Yukihiro Browse this author
Kinugawa, Shintaro Browse this author →KAKEN DB
Matsushima, Shouji Browse this author →KAKEN DB
Ono, Taisuke Browse this author
Sobirin, Mochamad A. Browse this author
Inoue, Naoki Browse this author
Yokota, Takashi Browse this author →KAKEN DB
Hirabayashi, Kagami Browse this author
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: skeletal muscle
myocardial infarction
apocynin
Issue Date: 2011
Publisher: American Physiological Society
Journal Title: American Journal of Physiology-Heart and Circulatory Physiology
Volume: 300
Issue: 5
Start Page: H1637
End Page: H1644
Publisher DOI: 10.1152/ajpheart.01185.2009
Abstract: Insulin resistance has been shown to occur as a consequence of heart failure. However, its exact mechanisms in this setting remain unknown. We have previously reported that oxidative stress is enhanced in the skeletal muscle from mice with heart failure after myocardial infarction (MI) (30). This study is aimed to investigate whether insulin resistance in postinfarct heart failure is due to the impairment of insulin signaling in the skeletal muscle caused by oxidative stress. Mice were divided into four groups: sham operated (sham); sham treated with apocynin, an inhibitor of NAD(P)H oxidase activation (10 mmol/l in drinking water); MI; and MI treated with apocynin. After 4 wk, intraperitoneal insulin tolerance tests were performed, and skeletal muscle samples were obtained for insulin signaling measurements. MI mice showed left ventricular dilation and dysfunction by echocardiography and increased left ventricular end-diastolic pressure and lung weight. The decrease in glucose level after insulin load significantly attenuated in MI compared with sham. Insulin-stimulated serine phosphorylation of Akt and glucose transporter-4 translocation were decreased in MI mice by 61 and 23%, respectively. Apocynin ameliorated the increase in oxidative stress and NAD(P)H oxidase activities measured by the lucigenin assay in the skeletal muscle after MI. It also improved insulin resistance and inhibited the decrease of Akt phosphorylation and glucose transporter-4 translocation. Insulin resistance was induced by the direct impairment of insulin signaling in the skeletal muscle from postinfarct heart failure, which was associated with the enhanced oxidative stress via NAD(P)H oxidase.
Type: article
URI: http://hdl.handle.net/2115/76766
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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