Adipose-Specific Knockout of raptor Results in Lean Mice with Enhanced Mitochondrial Respiration

被引：419

作者：

Polak, Pazit ^{[1
]}

Cybulski, Nadine ^{[1
]}

Feige, Jerome N. ^{[2
]}

Auwerx, Johan ^{[2
]}

Rueegg, Markus A. ^{[1
]}

Hall, Michael N. ^{[1
]}

机构：

[1] Univ Basel, Biozentrum, CH-4056 Basel, Switzerland

[2] Univ Strasbourg 1, INSERM, CNRS, Inst Clin Souris,Inst Genet & Biol Mol & Cellulai, F-67404 Illkirch Graffenstaden, France

来源：

CELL METABOLISM | 2008年 / 8卷 / 05期

基金：

瑞士国家科学基金会;

关键词：

D O I：

10.1016/j.cmet.2008.09.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

raptor is a specific and essential component of mammalian TOR complex 1 (mTORC1), a key regulator of cell growth and metabolism. To investigate a role of adipose mTORC1 in regulation of adipose and whole-body metabolism, we generated mice with an adipose-specific knockout of raptor (raptor(ad-/-)). Compared to control littermates, raptor(ad-1-) mice had substantially less adipose tissue, were protected against diet-induced obesity and hypercholesterolemia, and exhibited improved insulin sensitivity. Leanness was in spite of reduced physical activity and unaffected caloric intake, lipolysis, and absorption of lipids from the food. White adipose tissue of raptor(ad-/-) mice displayed enhanced expression of genes encoding mitochondrial uncoupling proteins characteristic of brown fat. Leanness of the raptorad-1- mice was attributed to elevated energy expenditure due to mitochondrial uncoupling. These results suggest that adipose mTORC1 is a regulator of adipose metabolism and, thereby, controls wholebody energy homeostasis.

引用

收藏

页码：399 / 410

页数：12

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