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

Heying Zhou, Yuichiro Yamada, Katsushi Tsukiyama, Kazumasa Miyawaki, Masaya Hosokawa, Kazuaki Nagashima, Kentaro Toyoda, Rei Naitoh, Wataru Mizunoya, Tohru Fushiki, Takashi Kadowaki, Yutaka Seino

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)937-942
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Sept 30 2005

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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