Author: ["Lei Sun","Huangming Xie","Marcelo A. Mori","Ryan Alexander","Bingbing Yuan","Shilpa M. Hattangadi","Qingqing Liu","C. Ronald Kahn","Harvey F. Lodish"]
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Abstract
PRDM16 is known to promote the differentiation of myoblastic progenitors to brown adipocytes. The miR-193b/365 microRNAs are shown to be induced by PRDM16 and promote brown fat differentiation, as well as block myogenesis. Mammals have two principal types of fat. White adipose tissue primarily serves to store extra energy as triglycerides, whereas brown adipose tissue is specialized to burn lipids for heat generation and energy expenditure as a defence against cold and obesity1,2. Recent studies have demonstrated that brown adipocytes arise in vivo from a Myf5-positive, myoblastic progenitor by the action of Prdm16 (PR domain containing 16). Here, we identified a brown-fat-enriched miRNA cluster, MiR-193b–365, as a key regulator of brown fat development. Blocking miR-193b and/or miR-365 in primary brown preadipocytes markedly impaired brown adipocyte adipogenesis by enhancing Runx1t1 (runt-related transcription factor 1; translocated to, 1) expression, whereas myogenic markers were significantly induced. Forced expression of Mir193b and/or Mir365 in C2C12 myoblasts blocked the entire programme of myogenesis, and, in adipogenic conditions, miR-193b induced myoblasts to differentiate into brown adipocytes. Mir193b–365 was upregulated by Prdm16 partially through Pparα. Our results demonstrate that Mir193b–365 serves as an essential regulator for brown fat differentiation, in part by repressing myogenesis.Cite this article
Sun, L., Xie, H., Mori, M. et al. Mir193b–365 is essential for brown fat differentiation. Nat Cell Biol 13, 958–965 (2011). https://doi.org/10.1038/ncb2286 