研究人员发现，小RNA家族中非编码小RNA促进了棕色脂肪组织的形成，新成果发表在7月在线出版的《自然—细胞生物学》期刊上。在哺乳类动物中，棕色脂肪能燃烧脂肪产生热量并可预防肥胖症，因此，新发现可用于开发治疗肥胖症和相关疾病的新方法。

棕色脂肪细胞也称为脂肪细胞，分化自可形成肌肉或脂肪的祖源细胞。Harvey Lodish和同事发现，在棕色脂肪的形成过程中，小RNA miR-193b和 miR-365的表达被上调了。他们指出，阻断这些小RNA的功能可阻止棕色脂肪的形成，同时诱导肌肉相关标记的表达。相反，诱导小RNA的表达则阻止了细胞中肌肉的分化并提高了棕色脂肪细胞的形成。

这些小RNA的功能需要在模式动物中进一步研究，以鉴别出对付肥胖症的治疗靶标。

原文出处：

Nature Cell Biology    doi:10.1038/ncb2286

Mir193b–365 is essential for brown fat differentiation

Lei Sun,Huangming Xie, Marcelo A. Mori, Ryan Alexander,Bingbing Yuan,Shilpa M. Hattangadi,Qingqing Liu,C. Ronald Kahn & Harvey F. Lodish

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.