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AMP‐activated protein kinase (AMPK) α1 is required for brown adipogenesis (LB843)
Author(s) -
Yang Qiyuan,
Liang Xingwei,
Fu Xing,
Rogers Carl,
Zhu Meijun,
Du Min
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb843
Subject(s) - adipogenesis , ampk , prdm16 , protein kinase a , amp activated protein kinase , endocrinology , chemistry , microbiology and biotechnology , medicine , brown adipose tissue , adipose tissue , biology , kinase
Brown adipose tissue (BAT) burns fatty acids to generate heat, holding the promise to treat obesity and type 2 diabetes. However, mechanisms regulating brown adipocyte formation remain poorly defined. AMP‐activated protein kinase (AMPK) is a key regulator of energy metabolism. We hypothesized that AMPK regulates the development of brown fat, an important organ involved in energy catabolism. To test, we employed AMPKα1 floxed mice which were crossed with ER‐Cre mice to conditionally knockout AMPKα1. AMPKα1 knockout was induced by 4‐hydrotamoxifen. Abrogation of AMPKα1 blunted the brown adipogenic differentiation of stromal vascular cells isolated from brown fat. Correspondingly, the expression of UCP‐1 and Prdm16, two markers of brown adipogenesis, was pronouncedly suppressed during differentiation (around 4 fold and 3 fold reduction respectively, P = 0.03). Moreover, adipogenic progenitor cells were separated from brown stromal vascular cells by FACS using surface markers (sca1+/CD34+/CD45‐). Consistently, the absence of AMPKα1 blocked brown adipogenesis in purified progenitors. Taken together, these data suggest that the AMPKα1 is required for brown adipogenesis (The work was funded by NIH R01HD067449). Grant Funding Source : Supported by NIH R01HD067449