Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10768777 | Biochemical and Biophysical Research Communications | 2005 | 6 Pages |
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-1â/âGIPRâ/â 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-1â/âGIPRâ/â 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.
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Authors
Heying Zhou, Yuichiro Yamada, Katsushi Tsukiyama, Kazumasa Miyawaki, Masaya Hosokawa, Kazuaki Nagashima, Kentaro Toyoda, Rei Naitoh, Wataru Mizunoya, Tohru Fushiki, Takashi Kadowaki, Yutaka Seino,