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dipocyte-specific deletion of mTOR inhibits adipose tissue development and causes insulin resistance in mice

编辑： 时间：2018年09月08日 访问次数:169

Adipocyte-specific deletion of mTOR inhibits adipose tissue development and causes insulin resistance in mice

Tizhong Shan（单体中）,1,2,* Pengpeng Zhang,2,3,* Qinyang Jiang,2,4,* Yan Xiong,2,* Yizhen Wang（汪以真）,1 and Shihuan Kuang2,5
1College of Animal Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, People’s Republic of China
2Department of Animal Sciences, Purdue University, 901 West State Street, West Lafayette, IN 47907, USA
3College of Life Sciences, Xinyang Normal University, Xinyang, People’s Republic of China
4College of animal science and technology, Guangxi University, Nanning, People’s Republic of China
5Purdue University Center for Cancer Research, West Lafayette, IN 47907, USA
Corresponding authors: Tizhong Shan, College of Animal Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, People’s Republic of China, nc.ude.ujz@nahszt. Shihuan Kuang, Department of Animal Sciences, Purdue University, 901 West State Street, West Lafayette, IN 47907, USA, ude.eudrup@gnauks

*Tizhong Shan, Pengpeng Zhang, Qinyang Jiang and Yan Xiong contributed equally to this paper.


期刊：DIABETOLOGIA

Impact Factor (影响因子): 6.08（2016年）

出版年：JUN 2016

摘要：The in vivo role of mechanistic target of rapamycin (mTOR) in the development and function of adipose tissue, especially brown adipose tissue (BAT), is not well understood. Here, we aimed to assess the effect of mTOR (also known as Mtor) knockout on adipose tissues and systemic energy metabolism. We generated adipocyte-specific mTOR-knockout mice (Adipoq-mTOR) by crossing adiponectin-Cre (Adipoq-Cre) mice with mTORflox/flox mice. The mice were then subjected to morphological, physiological (indirect calorimetry, glucose and insulin tolerance tests), and gene expression analyses to determine the role of mTOR in adipose tissues. We provide in vivo evidence that mTOR is essential for adipose tissue development and growth. Deletion of mTOR decreased the mass of both BAT and white adipose tissues (WAT) and induced browning of WAT. In addition, ablation of mTOR in adipose tissues caused insulin resistance and fatty liver in the Adipoq-mTOR mice. Furthermore, mTOR was required for adipocyte differentiation in vivo and PPARγ rescued the differentiation deficiency of the mTOR-null adipocytes. Our findings demonstrate that mTOR is a critical regulator of adipogenesis and systemic energy metabolism. Our study provides key insights into the role of mTOR in adipose tissues; such knowledge may facilitate the development of novel strategies with which to treat obesity and related metabolic diseases.