2. Academic Validation
  3. 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.
PMID: 31230984 DOI: 10.1016/j.cmet.2019.05.022
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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