内科学
内分泌学
食物摄入量
肥胖
P70-S6激酶1
减肥
体重
生物
信号转导
胰岛素
mTORC1型
能量稳态
葡萄糖稳态
瘦素
PI3K/AKT/mTOR通路
低蛋白饮食
体重增加
胰岛素抵抗
产矿性
雷帕霉素的作用靶点
胰岛素受体
医学
高蛋白饮食
碳水化合物代谢
饮食性肥胖
生酮饮食
作者
Yingga Wu,Baoguo Li,Li Li,Sharon E. Mitchell,Cara L Green,Giuseppe D'Agostino,Guanlin Wang,Lu Wang,Min Li,Jianbo Li,Chaoqun Niu,Zengguang Jin,Anyongqi Wang,Yu Zheng,Alex Douglas,John R. Speakman
出处
期刊:Cell Metabolism
[Elsevier]
日期:2021-05-04
卷期号:33 (5): 888-904.e6
被引量:14
标识
DOI:10.1016/j.cmet.2021.01.017
摘要
The protein leverage hypothesis predicts that low dietary protein should increase energy intake and cause adiposity. We designed 10 diets varying from 1% to 20% protein combined with either 60% or 20% fat. Contrasting the expectation, very low protein did not cause increased food intake. Although these mice had activated hunger signaling, they ate less food, resulting in decreased body weight and improved glucose tolerance but not increased frailty, even under 60% fat. Moreover, they did not show hyperphagia when returned to a 20% protein diet, which could be mimicked by treatment with rapamycin. Intracerebroventricular injection of AAV-S6K1 significantly blunted the decrease in both food intake and body weight in mice fed 1% protein, an effect not observed with inhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the 1% protein diet induced decreased food intake and body weight via a mechanism partially dependent on hypothalamic mTOR signaling.
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