Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action

被引：82

作者：

Zhou, HY

Yamada, Y ^{[1
]}

Tsukiyama, K

Miyawaki, K

Hosokawa, M

Nagashima, K

Toyoda, K

Naitoh, R

Mizunoya, W

Fushiki, T

Kadowaki, T

Seino, Y

机构：

[1] Kyoto Univ, Dept Diabet & Clin Nutr, Grad Sch Med, Kyoto, Japan

[2] Kyoto Univ, Grad Sch Agr, Div Food Sci & Biotechnol, Kyoto, Japan

[3] Univ Tokyo, Dept Metab Dis, Grad Sch Med, Tokyo, Japan

[4] Kansai Denryoku Hosp, Osaka, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 335卷 / 03期

关键词：

GIP; IRS-1; PPAR alpha; energy expenditure;

D O I：

10.1016/j.bbrc.2005.07.164

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)- 1-deficient mice and revealed that IRS-1(-/-) GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-) GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. (C) 2005 Elsevier Inc. All rights reserved.

引用

页码：937 / 942

页数：6

共 26 条

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