Study of GIPR signaling in adipose tissue under high-fat diet condition: Analysis of adipose tissue specific GIP receptor-deficient mice

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K16276
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Eating habits
• Research Institution: Kyoto University
• Principal Investigator: Matsunaga Erina (城尾恵里奈) 京都大学, 医学研究科, 特定研究員 (40737871)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: ＧＩＰ / インクレチン / 脂肪肝 / インスリン抵抗性 / 肥満

Outline of Final Research Achievements

GIP receptor (GIPR) directly induces energy accumulation in adipose tissue in vitro. However, the importance of the direct effect of GIPR signaling on adipose tissue in vivo remains unclear. In this study, we generated adipose tissue-specific GIPR knockout (KO) mice and investigated the direct actions of GIP in adipose tissue. Under high-fat diet (HFD)-fed conditions, KO mice had significantly lower body weight and lean body mass compared with those in floxed GIPR (WT) mice, although the fat volume was not significantly different between the two groups. Interestingly, insulin resistance, liver weight, and hepatic steatosis were reduced in HFD-fed KO mice. Plasma levels of interleukin-6 (IL-6), a proinflammatory cytokine that induces insulin resistance, were reduced in HFD-fed KO mice compared with those in HFD-fed WT mice. Thus, GIPR signaling in adipose tissue plays a critical role in HFD-induced insulin resistance and hepatic steatosis in vivo, which may involve IL-6 signaling.

Free Research Field

代謝栄養学