mTOR couples cellular nutrient sensing to organismal metabolic homeostasis

被引：286

作者：

Howell, Jessica J. ^{[1
]}

Manning, Brendan D. ^{[1
]}

机构：

[1] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2011年 / 22卷 / 03期

基金：

美国国家卫生研究院;

关键词：

DIET-INDUCED OBESITY; TUBEROUS SCLEROSIS COMPLEX-2; HEPATIC INSULIN-RESISTANCE; P70; S6; KINASE; MAMMALIAN TARGET; ADIPOCYTE DIFFERENTIATION; SKELETAL-MUSCLE; BODY-WEIGHT; FOOD-INTAKE; BETA-CELLS;

D O I：

10.1016/j.tem.2010.12.003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The mammalian target of rapamycin complex 1 (mTORC1) has the ability to sense a variety of essential nutrients and respond by altering cellular metabolic processes. Hence, this protein kinase complex is poised to influence adaptive changes to nutrient fluctuations toward the maintenance of whole-body metabolic homeostasis. Defects in mTORC1 regulation, arising from either physiological or genetic conditions, are believed to contribute to the metabolic dysfunction underlying a variety of human diseases, including type 2 diabetes. We are just now beginning to gain insights into the complex tissue-specific functions of mTORC1. In this review, we detail the current knowledge of the physiological functions of mTORC1 in controlling systemic metabolism, with a focus on advances obtained through genetic mouse models.

引用

页码：94 / 102

页数：9

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