Loss of Akt1 in mice increases energy expenditure and protects against diet-induced obesity.

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