小柯机器人

美国凯斯西储大学Atul R. Chopra课题组发现，蛋白酪氨酸磷酸酶受体δ是促食性asprosin的受体。这一研究成果于2022年3月16日在线发表在国际学术期刊《细胞—代谢》上。

研究人员确定了蛋白酪氨酸磷酸酶受体δ（Ptprd）是asprosin的促食受体。asprosin在下丘脑AgRP神经元中作为高亲和力的Ptprd配体发挥作用，以细胞自主的方式调控该回路的活性。Ptprd的基因敲除导致强烈的食欲减退、瘦弱和不能对asprosin的促食作用作出反应。在AgRP神经元中特异性地敲除Ptprd会导致对饮食引起的肥胖的抵抗。在小鼠的血液循环中引入可溶性Ptprd配体结合域，通过封存血浆中的asprosin来抑制食欲和血糖水平。研究人员将Ptprd鉴定为促食asprosin受体，这为开发抗肥胖治疗药物创造了一个新的途径。

据悉，asprosin是一种空腹诱导的致糖性和中枢作用的促食激素。已知嗅觉受体Olfr734是asprosin的肝脏受体，介导其对葡萄糖产生的影响，但asprosin的促食功能的受体一直不清楚。

附：英文原文

Title: Protein tyrosine phosphatase receptor δ serves as the orexigenic asprosin receptor

Author: Ila Mishra, Wei Rose Xie, Juan C. Bournat, Yang He, Chunmei Wang, Elizabeth Sabath Silva, Hailan Liu, Zhiqiang Ku, Yinghua Chen, Bernadette O. Erokwu, Peilin Jia, Zhongming Zhao, Zhiqiang An, Chris A. Flask, Yanlin He, Yong Xu, Atul R. Chopra

Issue&Volume: 2022-03-16

Abstract: Asprosin is a fasting-induced glucogenic and centrally acting orexigenic hormone.The olfactory receptor Olfr734 is known to be the hepatic receptor for asprosin thatmediates its effects on glucose production, but the receptor for asprosin’s orexigenicfunction has been unclear. Here, we have identified protein tyrosine phosphatase receptorδ (Ptprd) as the orexigenic receptor for asprosin. Asprosin functions as a high-affinityPtprd ligand in hypothalamic AgRP neurons, regulating the activity of this circuitin a cell-autonomous manner. Genetic ablation of Ptprd results in a strong loss of appetite, leanness, and an inability to respond to theorexigenic effects of asprosin. Ablation of Ptprd specifically in AgRP neurons causes resistance to diet-induced obesity. Introductionof the soluble Ptprd ligand-binding domain in the circulation of mice suppresses appetiteand blood glucose levels by sequestering plasma asprosin. Identification of Ptprdas the orexigenic asprosin receptor creates a new avenue for the development of anti-obesitytherapeutics.

DOI: 10.1016/j.cmet.2022.02.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00084-5

Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
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