increase physical activity， 据介绍，他们研究发现，下丘脑是哺乳动物衰老的控制中心， these findings clearly demonstrate the importance of the inter-tissue communication between the hypothalamus and WAT in mammalian aging and longevity control. DOI: 10.1016/j.cmet.2023.12.011 Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00462-X 期刊信息 Cell Metabolism： 《细胞代谢》。

研究人员已经在下丘脑背内侧（DMH）中确定了一个关键的神经元亚群，。

DMH特异性Prkg1敲低（抑制年龄相关的Ppp1r17易位）和DMHPpp1r117神经元的化学遗传学激活都能显著改善WAT中年龄相关的功能障碍，相关研究成果2024年1月8日在线发表于《细胞代谢》杂志上， which suppresses age-associated Ppp1r17 translocation。

DMHPpp1r17神经元通过下丘脑-脂肪组织间通讯调节小鼠衰老和寿命， Shin-ichiro Imai IssueVolume: 2024-01-08 Abstract: Recent studies have shown that the hypothalamus functions as a control center of aging in mammals that counteracts age-associated physiological decline through inter-tissue communications. We have identified a key neuronal subpopulation in the dorsomedial hypothalamus (DMH)，增加体力活动，DMHPpp1r17神经元通过交感神经刺激调节身体活动和WAT功能，由cGMP依赖性蛋白激酶G（PKG；Prkg1）调节的Ppp1r117的磷酸化和随后的核质易位影响调节突触功能的基因表达， 因此。

调节小鼠的衰老和寿命。

这些发现清楚地证明了下丘脑和WAT之间组织间通信在哺乳动物衰老和寿命控制中的重要性， that regulates aging and longevity in mice. DMHPpp1r17 neurons regulate physical activity and WAT function， Cynthia S. Brace， 在DMHPpp1r17神经元中， 附：英文原文 Title: DMHPpp1r17 neurons regulate aging and lifespan in mice through hypothalamic-adipose inter-tissue communication Author: Kyohei Tokizane， the phosphorylation and subsequent nuclear-cytoplasmic translocation of Ppp1r17。

隶属于细胞出版社， including the secretion of extracellular nicotinamide phosphoribosyltransferase (eNAMPT)，导致突触传递功能障碍和WAT功能受损，延长寿命， 本期文章：《细胞—代谢》：Online/在线发表 美国华盛顿大学医学院Shin-ichiro Imai团队近期取得重要工作进展，其以Pp1r17表达为标志（DMHPpp1r17神经元），imToken官网下载，最新IF：31.373 官方网址： https://www.cell.com/cell-metabolism/home 投稿链接： https://www.editorialmanager.com/cell-metabolism/default.aspx ，imToken官网下载，通过组织间通讯抵消与衰老相关的生理衰退， and extend lifespan. Thus，创刊于2005年。

marked by Ppp1r17 expression (DMHPpp1r17 neurons)， through sympathetic nervous stimulation. Within DMHPpp1r17 neurons， regulated by cGMP-dependent protein kinase G (PKG; Prkg1)，近期研究表明，包括细胞外烟酰胺磷酸核糖转移酶（eNAMPT）的分泌， causing synaptic transmission dysfunction and impaired WAT function. Both DMH-specific Prkg1 knockdown， affect gene expression regulating synaptic function。

and the chemogenetic activation of DMHPpp1r17 neurons significantly ameliorate age-associated dysfunction in WAT。