Journal
NATURE COMMUNICATIONS
Volume 10, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-12988-8
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Funding
- National Natural Science Foundation of China [91749103, 81421061, 31100624, 81200586]
- National Major Fundamental Research 973 Program of China [2014CB942902]
- NIH [R01CA31534]
- Cancer Prevention Research Institute of Texas [RP120348, RP120459]
- Marie Betzner Morrow Centennial Endowment
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beta-Adrenergic receptor (beta-AR) signaling is a pathway controlling adaptive thermogenesis in brown or beige adipocytes. Here we investigate the biological roles of the transcription factor Foxp1 in brown/beige adipocyte differentiation and thermogenesis. Adipose-specific deletion of Foxp1 leads to an increase of brown adipose activity and browning program of white adipose tissues. The Foxp1-deficient mice show an augmented energy expenditure and are protected from diet-induced obesity and insulin resistance. Consistently, overexpression of Foxp1 in adipocytes impairs adaptive thermogenesis and promotes diet-induced obesity. A robust change in abundance of the beta 3-adrenergic receptor (beta 3-AR) is observed in brown/beige adipocytes from both lines of mice. Molecularly, Foxp1 directly represses beta 3-AR transcription and regulates its desensitization behavior. Taken together, our findings reveal Foxp1 as a master transcriptional repressor of brown/beige adipocyte differentiation and thermogenesis, and provide an important clue for its targeting and treatment of obesity.
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