mTOR couples cellular nutrient sensing to organismal metabolic homeostasis

被引:287
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
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
收藏
页码:94 / 102
页数:9
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