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蛋白质含量极低的饮食会导致食物摄入减少和体重减轻
作者:小柯机器人 发布时间:2021/3/7 22:21:03

中国科学院遗传与发育生物学研究所John R. Speakman研究组发现,蛋白质含量极低的饮食会导致食物摄入减少和体重减轻,并与抑制下丘脑mTOR信号传导有关。2021年3月4日出版的《细胞—代谢》发表了这项成果。

研究人员设计了10种饮食,蛋白质含量从1%到20%不等,再加上60%或20%的脂肪,这与人们预期的超低蛋白质不会导致食物摄入增加有关。尽管这些小鼠具有激活的饥饿信号,但它们吃的食物更少,导致体重减轻和葡萄糖耐量提高,但即使在脂肪含量低于60%的情况下,其脆弱性也没有增加。

而且,当它们恢复到20%的蛋白质饮食时,并没有表现出食欲亢进,这可以通过雷帕霉素治疗来模拟。脑室内注射AAV-S6K1明显抑制了喂食1%蛋白小鼠的食物摄入和体重的减少,但对eIF2a、TRPML1和Fgf21信号的抑制未观察到这种作用。因此,1%蛋白质饮食通过部分依赖下丘脑mTOR信号传导的机制诱导食物摄取和体重减少。 

据了解,蛋白质杠杆假说预测低膳食蛋白会增加能量摄入并引起肥胖。

附:英文原文

Title: Very-low-protein diets lead to reduced food intake and weight loss, linked to inhibition of hypothalamic mTOR signaling, in mice

Author: 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

Issue&Volume: 2021-03-04

Abstract: The protein leverage hypothesis predicts that low dietary protein should increaseenergy intake and cause adiposity. We designed 10 diets varying from 1% to 20% proteincombined with either 60% or 20% fat, contrasting the expectation that very low proteindid not cause increased food intake. Although these mice had activated hunger signaling,they ate less food, resulting in decreased body weight and improved glucose tolerancebut not increased frailty, even under 60% fat. Moreover, they did not show hyperphagiawhen returned to a 20% protein diet, which could be mimicked by treatment with rapamycin.Intracerebroventricular injection of AAV-S6K1 significantly blunted the decrease inboth food intake and body weight in mice fed 1% protein, an effect not observed withinhibition of eIF2a, TRPML1, and Fgf21 signaling. Hence, the 1% protein diet induceddecreased food intake and body weight via a mechanism partially dependent on hypothalamicmTOR signaling.

DOI: 10.1016/j.cmet.2021.01.017

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00017-6

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx