期刊论文详细信息
MOLECULAR AND CELLULAR ENDOCRINOLOGY 卷:439
Ablation of PPP1R3G reduces glycogen deposition and mitigates high-fat diet induced obesity
Article
Zhang, Yongxian1  Gu, Jin1  Wang, Lin1  Zhao, Zilong1  Pan, Yi1  Chen, Yan1 
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, CAS Key Lab Nutr & Metab, Shanghai 200031, Peoples R China
关键词: Glycogen;    Obesity;    Insulin resistance;    Hepatic steatosis;    Adipocytes;   
DOI  :  10.1016/j.mce.2016.10.036
来源: Elsevier
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【 摘 要 】

Glycogen and triglyceride are two major forms of energy storage in the body and provide the fuel during different phases of food deprivation. However, how glycogen metabolism is linked to fat deposition in adipose tissue has not been clearly characterized. We generated a mouse model with whole-body deletion of PPP1R3G, a glycogen-targeting subunit of protein phosphatase-1 required for glycogen synthesis. Upon feeding with high-fat diet, the body weight and fat composition are significantly reduced in the PPP1R3G(-/-) mice compared to the wild type controls. The metabolic rate of the mice as measured by O-2 consumption and CO2 production is accelerated by PPPIR3G deletion. The high-fat diet-induced liver steatosis is also slightly relieved by PPP1R3G deletion. The glycogen level in adipose tissue is reduced by PPP1R3G deletion. In 3T3L1 cells, overexpression of PPPIR3G leads to increases of both glycogen and triglyceride levels. In conclusion, our study indicates that glycogen is actively involved in fat accumulation in adipose tissue and obesity development upon high-fat diet. Our study also suggests that PPP1R3G is an important player that links glycogen metabolism to lipid metabolism in vivo. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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