1. Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action
- Author
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Zhou, Heying, Yamada, Yuichiro, Tsukiyama, Katsushi, Miyawaki, Kazumasa, Hosokawa, Masaya, Nagashima, Kazuaki, Toyoda, Kentaro, Naitoh, Rei, Mizunoya, Wataru, Fushiki, Tohru, Kadowaki, Takashi, and Seino, Yutaka
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GROWTH factors , *OBESITY , *FAT , *INSULIN - Abstract
Abstract: Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic β-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. [Copyright &y& Elsevier]
- Published
- 2005
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