2019年8月出版的国际学术期刊《细胞—代谢》发表了清华大学王一国研究团队的研究。他们发现OLFR734可以作为一类新型葡萄糖代谢调节剂。

该研究组已经确定嗅觉受体OLFR734作为一类白脂素受体可调节肝脏葡萄糖的生成。OLFR734敲除小鼠对白脂素的反应减弱，包括cAMP水平降低，肝葡萄糖生成减少，以及胰岛素敏感性提高。由于OLFR734缺乏会显著降低空腹和高脂饮食诱导的葡萄糖生成，研究结果表明，OLFR734作为白脂素受体，在饥饿和肥胖的情况下对维持机体的葡萄糖稳态发挥着关键作用。

据了解，白脂素是一种由饥饿引起的激素，通过一种未知的G蛋白偶联受体（GPCR）激活cAMP信号通路，促使肝脏生成葡萄糖，并刺激下丘脑食欲。然而，白脂素的真正受体尚未清楚。
 

更多阅读：

随着经济的快速发展以及人们生活方式的改变，2型糖尿病成为严重影响人们健康和生活质量的重要疾病，其典型特征是血液中葡萄糖浓度的升高。该研究首次确定了嗅觉受体OLFR734作为Asprosin的受体在饥饿和肥胖情况下对维持机体葡萄糖稳态的关键作用，拓展了嗅觉受体的非嗅觉功能，为糖尿病的治疗提供了一个潜在的药物靶点。（据清华大学新闻网）

附：英文原文

Title: OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin

Author: Erwei Li, Haili Shan, Liqun Chen, Aijun Long, Yuanyuan Zhang, Yang Liu, Liangjie Jia, Fangchao Wei, Jinbo Han, Tong Li, Xiaohui Liu, Haiteng Deng, Yiguo Wang

Issue&Volume: Volume 30 Issue 2

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.

DOI: https://doi.org/10.1016/j.cmet.2019.05.022

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30262-1