Loss of Akt1 in Mice Increases Energy Expenditure and Protects against Diet-Induced Obesity

被引：63

作者：

Wan, Min ^{[1
]}

Easton, Rachael M. ^{[1
]}

Gleason, Catherine E. ^{[1
]}

Monks, Bobby R. ^{[1
]}

Ueki, Kohjiro ^{[2
]}

Kahn, C. Ronald ^{[3
]}

Birnbaum, Morris J. ^{[1
]}

机构：

[1] Univ Penn, Inst Diabet Obes & Metab, Philadelphia, PA 19104 USA

[2] Univ Tokyo, Grad Sch Med, Tokyo, Japan

[3] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2012年 / 32卷 / 01期

关键词：

BROWN ADIPOSE-TISSUE; SKELETAL-MUSCLE; GLUCOSE-HOMEOSTASIS; INSULIN-RESISTANCE; UNCOUPLING PROTEIN-3; KINASE-B; METABOLIC SYNDROME; HEPATIC STEATOSIS; EXERCISE; LACKING;

D O I：

10.1128/MCB.05806-11

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Akt is encoded by a gene family for which each isoform serves distinct but overlapping functions. Based on the phenotypes of the germ line gene disruptions, Akt1 has been associated with control of growth, whereas Akt2 has been linked to metabolic regulation. Here we show that Akt1 serves an unexpected role in the regulation of energy metabolism, as mice deficient for Akt1 exhibit protection from diet-induced obesity and its associated insulin resistance. Although skeletal muscle contributes most of the resting and exercising energy expenditure, muscle-specific deletion of Akt1 does not recapitulate the phenotype, indicating that the role of Akt1 in skeletal muscle is cell nonautonomous. These data indicate a previously unknown function of Akt1 in energy metabolism and provide a novel target for treatment of obesity.

引用

页码：96 / 106

页数：11

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