TY - JOUR
T1 - Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action
AU - Zhou, Heying
AU - Yamada, Yuichiro
AU - Tsukiyama, Katsushi
AU - Miyawaki, Kazumasa
AU - Hosokawa, Masaya
AU - Nagashima, Kazuaki
AU - Toyoda, Kentaro
AU - Naitoh, Rei
AU - Mizunoya, Wataru
AU - Fushiki, Tohru
AU - Kadowaki, Takashi
AU - Seino, Yutaka
N1 - Funding Information:
This study was supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan, and by Health Sciences Research Grants for Comprehensive Research on Aging and Health from the Ministry of Health, Labor and Welfare, Japan.
PY - 2005/9/30
Y1 - 2005/9/30
N2 - 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.
AB - 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.
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U2 - 10.1016/j.bbrc.2005.07.164
DO - 10.1016/j.bbrc.2005.07.164
M3 - Article
C2 - 16105663
AN - SCOPUS:23944463919
SN - 0006-291X
VL - 335
SP - 937
EP - 942
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -
