| First Author | Zhou H | Year | 2005 |
| Journal | Biochem Biophys Res Commun | Volume | 335 |
| Issue | 3 | Pages | 937-42 |
| PubMed ID | 16105663 | Mgi Jnum | J:100642 |
| Mgi Id | MGI:3589049 | Doi | 10.1016/j.bbrc.2005.07.164 |
| Citation | Zhou H, et al. (2005) Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. Biochem Biophys Res Commun 335(3):937-42 |
| abstractText | 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. |
