HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

(Pro)renin receptor in skeletal muscle is involved in the development of insulin resistance associated with postinfarct heart failure in mice

Files in This Item:

The file(s) associated with this item can be obtained from the following URL:https://doi.org/10.1152/ajpendo.00449.2013


Title: (Pro)renin receptor in skeletal muscle is involved in the development of insulin resistance associated with postinfarct heart failure in mice
Authors: Fukushima, Arata Browse this author →KAKEN DB
Kinugawa, Shintaro Browse this author →KAKEN DB
Takada, Shingo Browse this author →KAKEN DB
Matsushima, Shouji Browse this author →KAKEN DB
Sobirin, Mochamad Ali Browse this author
Ono, Taisuke Browse this author
Takahashi, Masashige Browse this author
Suga, Tadashi Browse this author
Homma, Tsuneaki Browse this author
Masaki, Yoshihiro Browse this author
Furihata, Takaaki Browse this author
Kadoguchi, Tomoyasu Browse this author
Yokota, Takashi Browse this author →KAKEN DB
Okita, Koichi Browse this author →KAKEN DB
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: (pro)renin receptor
renin-angiotensin system
oxidative stress
insulin resistance
heart failure
Issue Date: 2014
Publisher: American Physiological Society
Journal Title: American Journal of Physiology-Endocrinology and Metabolism
Volume: 307
Issue: 6
Start Page: E503
End Page: E514
Publisher DOI: 10.1152/ajpendo.00449.2013
Abstract: We previously reported that insulin resistance was induced by the impairment of insulin signaling in the skeletal muscle from heart failure (HF) via NAD(P)H oxidase-dependent oxidative stress. (Pro)renin receptor [(P)RR] is involved in the activation of local renin-angiotensin system and subsequent oxidative stress. We thus examined whether (P)RR inhibitor, handle region peptide (HRP), could ameliorate insulin resistance in HF after myocardial infarction (MI) by improving oxidative stress and insulin signaling in the skeletal muscle. C57BL6J mice were divided into four groups: sham operated (Sham, n = 10), Sham treated with HRP (Sham+HRP, 0.1 mg·kg−1·day−1, n = 10), MI operated (MI, n = 10), and MI treated with HRP (MI+HRP, 0.1 mg/kg/day, n = 10). After 4 wk, MI mice showed left ventricular dysfunction, which was not affected by HRP. (P)RR was upregulated in the skeletal muscle after MI (149% of sham, P < 0.05). The decrease in plasma glucose after insulin load was smaller in MI than in Sham (21 ± 2 vs. 44 ± 3%, P < 0.05), and was greater in MI+HRP (38 ± 2%, P < 0.05) than in MI. Insulin-stimulated serine phosphorylation of Akt and glucose transporter 4 translocation were decreased in the skeletal muscle from MI by 48 and 49% of Sham, both of which were ameliorated in MI+HRP. Superoxide production and NAD(P)H oxidase activities were increased in MI, which was inhibited in MI+HRP. HRP ameliorated insulin resistance associated with HF by improving insulin signaling via the inhibition of NAD(P)H oxidase-induced superoxide production in the skeletal muscle. The (P)RR pathway is involved in the development of insulin resistance, at least in part, via the impairment of insulin signaling in the skeletal muscle from HF.
Type: article
URI: http://hdl.handle.net/2115/76770
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)

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 

 - Hokkaido University