营养过剩
内分泌学
内科学
辅活化剂
福克斯O1
生物
受体
调节器
能源消耗
下调和上调
磷酸化
细胞生物学
基因
医学
转录因子
遗传学
蛋白激酶B
肥胖
作者
Yongjie Yang,Yanlin He,Hailan Liu,Wenjun Zhou,Chunmei Wang,Pingwen Xu,Xing Cai,Kaifan Yu,Pei Zhou,Ilirjana Hyseni,Makoto Fukuda,Qingchun Tong,Jianming Xu,Zheng Sun,Bert W. O’Malley,Yong Xu
出处
期刊:Cell Reports
[Elsevier]
日期:2021-12-01
卷期号:37 (10): 110075-110075
被引量:8
标识
DOI:10.1016/j.celrep.2021.110075
摘要
The neuroendocrine system coordinates metabolic and behavioral adaptations to fasting, including reducing energy expenditure, promoting counterregulation, and suppressing satiation and anxiety to engage refeeding. Here, we show that steroid receptor coactivator-2 (SRC-2) in pro-opiomelanocortin (POMC) neurons is a key regulator of all these responses to fasting. POMC-specific deletion of SRC-2 enhances the basal excitability of POMC neurons; mutant mice fail to efficiently suppress energy expenditure during food deprivation. SRC-2 deficiency blunts electric responses of POMC neurons to glucose fluctuations, causing impaired counterregulation. When food becomes available, these mutant mice show insufficient refeeding associated with enhanced satiation and discoordination of anxiety and food-seeking behavior. SRC-2 coactivates Forkhead box protein O1 (FoxO1) to suppress POMC gene expression. POMC-specific deletion of SRC-2 protects mice from weight gain induced by an obesogenic diet feeding and/or FoxO1 overexpression. Collectively, we identify SRC-2 as a key molecule that coordinates multifaceted adaptive responses to food shortage.
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