MicroRNA-378 controls classical brown fat expansion to counteract obesity

Dongning Pan, Chunxiao Mao, Brian Quattrochi, Randall H. Friedline, Lihua J. Zhu, Dae Young Jung, Jason K. Kim, Brian Lewis and Yong-Xu Wang ()
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Dongning Pan: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School
Chunxiao Mao: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School
Brian Quattrochi: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School
Randall H. Friedline: University of Massachusetts Medical School
Lihua J. Zhu: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School
Dae Young Jung: University of Massachusetts Medical School
Jason K. Kim: University of Massachusetts Medical School
Brian Lewis: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School
Yong-Xu Wang: Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Both classical brown adipocytes and brown-like beige adipocytes are considered as promising therapeutic targets for obesity; however, their development, relative importance and functional coordination are not well understood. Here we show that a modest expression of miR-378/378* in adipose tissue specifically increases classical brown fat (BAT) mass, but not white fat (WAT) mass. Remarkably, BAT expansion, rather than miR-378 per se, suppresses formation of beige adipocytes in subcutaneous WAT. Despite this negative feedback, the expanded BAT depot is sufficient to prevent both genetic and high-fat diet-induced obesity. At the molecular level, we find that miR-378 targets phosphodiesterase Pde1b in BAT but not in WAT. Indeed, miR-378 and Pde1b inversely regulate brown adipogenesis in vitro in the absence of phosphodiesterase inhibitor isobutylmethylxanthine. Our work identifies miR-378 as a key regulatory component underlying classical BAT-specific expansion and obesity resistance, and adds novel insights into the physiological crosstalk between BAT and WAT.

Date: 2014
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DOI: 10.1038/ncomms5725

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