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

Ohta, Yukihiro; Kinugawa, Shintaro; Matsushima, Shouji; Ono, Taisuke; Sobirin, Mochamad A.; Inoue, Naoki; Yokota, Takashi; Hirabayashi, Kagami; Tsutsui, Hiroyuki

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

Ohta, Yukihiro; Kinugawa, Shintaro; Matsushima, Shouji et al.

American Journal of Physiology-Heart and Circulatory Physiology, 2011, 300(5), H1637-H1644

Permalink : https://hdl.handle.net/2115/76766

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https://doi.org/10.1152/ajpheart.01185.2009			24

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アクセス権	open access
URI	https://hdl.handle.net/2115/76766
タイトル	Oxidative stress impairs insulin signal in skeletal muscle and causes insulin resistance in postinfarct heart failure
著者	Ohta, Yukihiro ; Kinugawa, Shintaro ; Matsushima, Shouji ; Ono, Taisuke ; Sobirin, Mochamad A. ; Inoue, Naoki ; Yokota, Takashi ; Hirabayashi, Kagami ; Tsutsui, Hiroyuki
著者名 Ohta, Yukihiro
e-Rad_Researcher 60399871 著者名 Kinugawa, Shintaro
e-Rad_Researcher 80552869 著者名 Matsushima, Shouji
著者名 Ono, Taisuke
著者名 Sobirin, Mochamad A.
著者名 Inoue, Naoki
e-Rad_Researcher 90374321 著者名 Yokota, Takashi
著者名 Hirabayashi, Kagami
e-Rad_Researcher 70264017 著者名 Tsutsui, Hiroyuki
言語	英語
キーワード	skeletal muscle
	myocardial infarction
	apocynin
発行日	2011
出版者	American Physiological Society
収録物名	American Journal of Physiology-Heart and Circulatory Physiology
巻(号)	300(5)
ページ	H1637-H1644
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
PISSN	0363-6135
EISSN	1522-1539
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1152/ajpheart.01185.2009