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首页> 外文期刊>Cell metabolism >MicroRNA-133 controls brown adipose determination in skeletal muscle satellite cells by targeting Prdm16
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MicroRNA-133 controls brown adipose determination in skeletal muscle satellite cells by targeting Prdm16

机译:MicroRNA-133通过靶向Prdm16控制骨骼肌卫星细胞中棕色脂肪的测定

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摘要

Brown adipose tissue (BAT) is an energy-dispensing thermogenic tissue that plays an important role in balancing energy metabolism. Lineage-tracing experiments indicate that brown adipocytes are derived from myogenic progenitors during embryonic development. However, adult skeletal muscle stem cells (satellite cells) have long been considered uniformly determined toward the myogenic lineage. Here, we report that adult satellite cells give rise to brown adipocytes and that microRNA-133 regulates the choice between myogenic and brown adipose determination by targeting the 3′UTR of Prdm16. Antagonism of microRNA-133 during muscle regeneration increases uncoupled respiration, glucose uptake, and thermogenesis in local treated muscle and augments whole-body energy expenditure, improves glucose tolerance, and impedes the development of diet-induced obesity. Finally, we demonstrate that miR-133 levels are downregulated in mice exposed to cold, resulting in de novo generation of satellite cell-derived brown adipocytes. Therefore, microRNA-133 represents an important therapeutic target for the treatment of obesity.
机译:棕色脂肪组织(BAT)是能量分配的生热组织,在平衡能量代谢中起重要作用。谱系追踪实验表明,棕色脂肪细胞在胚胎发育过程中源自成肌祖细胞。但是,长期以来一直认为成年骨骼肌干细胞(卫星细胞)是朝着成肌谱系统一确定的。在这里,我们报道了成年卫星细胞产生褐色脂肪细胞,而microRNA-133通过靶向Prdm16的3'UTR调节生肌和褐色脂肪测定之间的选择。在肌肉再生过程中,microRNA-133的拮抗作用增加了局部处理的肌肉的非耦合呼吸,葡萄糖摄取和生热作用,并增加了全身能量消耗,改善了葡萄糖耐量,并阻碍了饮食引起的肥胖症的发展。最后,我们证明在暴露于寒冷的小鼠中miR-133水平下调,导致卫星细胞衍生的棕色脂肪细胞从头产生。因此,microRNA-133代表了肥胖症的重要治疗靶标。

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