| First Author | Li E | Year | 2019 |
| Journal | Cell Metab | Volume | 30 |
| Issue | 2 | Pages | 319-328.e8 |
| PubMed ID | 31230984 | Mgi Jnum | J:279017 |
| Mgi Id | MGI:6357396 | Doi | 10.1016/j.cmet.2019.05.022 |
| Citation | Li E, et al. (2019) OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin. Cell Metab 30(2):319-328.e8 |
| abstractText | 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. |
