1. Academic Validation
  2. OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin

OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin

  • Cell Metab. 2019 Aug 6;30(2):319-328.e8. doi: 10.1016/j.cmet.2019.05.022.
Erwei Li 1 Haili Shan 1 Liqun Chen 1 Aijun Long 1 Yuanyuan Zhang 1 Yang Liu 1 Liangjie Jia 1 Fangchao Wei 1 Jinbo Han 1 Tong Li 1 Xiaohui Liu 2 Haiteng Deng 3 Yiguo Wang 4
Affiliations

Affiliations

  • 1 MOE Key Laboratory of Bioinformatics, Tsinghua-Peking Joint Center for Life Sciences, School of Life Sciences, Tsinghua University, 100084 Beijing, China.
  • 2 National Protein Science Technology Center, Tsinghua University, 100084 Beijing, China.
  • 3 MOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, 100084 Beijing, China.
  • 4 MOE Key Laboratory of Bioinformatics, Tsinghua-Peking Joint Center for Life Sciences, School of Life Sciences, Tsinghua University, 100084 Beijing, China. Electronic address: yiguo@mail.tsinghua.edu.cn.
Abstract

Asprosin is a fasting-induced hormone that promotes glucose production in the liver and stimulates appetite in the hypothalamus by activating the cAMP signaling pathway via an unknown G protein-coupled receptor (GPCR). However, the bona fide receptor of Asprosin is unclear. Here, we have identified that the olfactory receptor OLFR734 acts as a receptor of Asprosin to modulate hepatic glucose production. Olfr734 knockout mice show a blunted response to Asprosin, including attenuated cAMP levels and hepatic glucose production, and improved Insulin sensitivity. As Olfr734 deficiency dramatically attenuates both fasting and high-fat-diet-induced glucose production, our results demonstrate a critical role of OLFR734 as a receptor of Asprosin to maintain glucose homeostasis during fasting and in obesity.

Keywords

OLFR734; asprosin; cAMP; gluconeogenesis.

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