期刊
ENDOCRINOLOGY
卷 158, 期 3, 页码 578-591出版社
ENDOCRINE SOC
DOI: 10.1210/en.2016-1581
关键词
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资金
- National Natural Science Foundation [81471083, 81070680, 81500673, 81400844]
- Huashan Hospital, Fudan University [2013QD10]
- Shanghai Municipal Commission of Health and Family Planning [20144Y0070]
Obesity has become the most common metabolic disorder worldwide. Promoting brown adipose tissue (BAT) and beige adipose tissue formation, and therefore, a functional increase in energy expenditure, may counteract obesity. Mice lacking type II beta regulatory subunit of adenosine 3',5' cyclic monophosphate(cAMP)-dependent protein kinase A (PKA-RIIB) display reduced adiposity and resistance to diet-induced obesity. PKA-RIIB, encoded by the Prkar2b gene, is most abundant in BAT and white adipose tissue (WAT) and in the brain. In this study, we show that mice lacking PKARIIB have increased energy expenditure, limited weight gain, and improved glucose metabolism. PKA-RIIB deficiency induces brownlike adipocyte in inguinal WAT (iWAT). PKA-RIIB deficiency also increases the expression of uncoupling protein 1 and other thermogenic genes in iWAT and primary preadipocytes from iWAT through a mechanism involving increased PKA activity, which is represented by increased phosphorylation of PKA substrate, cAMP response element binding protein, and P38 mitogen-activated protein kinase. Our study provides evidence for the role of PKA-RIIB deficiency in regulating thermogenesis in WAT, which may potentially have therapeutic implications for the treatment of obesity and related metabolic disorders.
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