Browning of white adipocytes (beiging) is an attractive therapeutic strategy against obesity attributed to the enhanced capacity of heat production. Betatrophin as a novel cold-derived adipokines, is necessary for adipogenesis. Recent data suggest that Betatrophin deficient mice displayed increased thermogenesis and reduced body weight. But its role in the browning of white adipocytes remains unknown. Here, we report that deletion of Betatrophin in 3T3-L1 adipocytes enhanced expression of brown fat-specific markers (UCP-1, PRDM16 and CIDEA), mitochondrial biogenesis genes (PGC-1α) and the key lipid metabolism lipases (ATGL), Additionally, those effects were dramatically abolished by compound C, revealing silencing Betatrophin-induced browning depend on activation of AMPK signaling pathways. Overall, our findings suggest that Betatrophin is a candidate target gene treating obesity due to its function of inhibiting white adipocyte browning conversion.

Disclosure

X. Qi: None. Z. Liao: None. Y. Wang: None. J. Li: None. J. Liu: None. X. Xiao: None.

© 2019 by the American Diabetes Association.
2019
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