GRK5 deficiency decreases diet-induced obesity and adipogenesis

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• 作者：Feifei Wang¹ ; Li Wang¹ ; Minjie Shen ; Lan Ma ; ^{lanma@shmu.edu.cn}
• 关键词：ANOVA ; analysis of variance ; GPCR ; G protein&ndash ; coupled receptor ; GRK ; GPCR kinase ; KO ; knockout ; SD ; standard diet ; HFD ; high fat diet ; WAT ; white adipose tissue ; MEF ; mouse embryonic fibroblast ; SVF ; stromal vascular fraction cell ; PPAR纬 ; peroxisome
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：4 May, 2012
• 卷：421
• 期：2
• 页码：312-317
• 文件大小：676 K

摘要

Identification of the protein factors that regulate the adipogenesis and lipid metabolism of adipose tissue is critical for the understanding of the physiology and pathology of obesity and energy homeostasis. In this study, we found that G protein coupled receptor (GPCR) kinase 5 (GRK5) was expressed at a relatively high level in the white adipose tissue. When fed on a high-fat diet, GRK5^{鈭?鈭?/sup> mice gained significantly less weight and had decreased WAT mass than their wild type littermates, which could not be attributed to alterations in food consumption or energy expenditure. However, GRK5鈭?鈭?/sup> mice showed a 30-70%decreased expression of lipid metabolism and adipogenic genes in WAT. Moreover, GRK5鈭?鈭?/sup> embryonic fibroblasts and preadipocytes exhibited 40-70%decreased expression of adipogenic genes and impaired adipocyte differentiation when induced in vitro. Taken together, these results suggest that GRK5 is an important regulator of adipogenesis and is crucial for the development of diet-induced obesity.}