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首页> 外文期刊>Journal of Cellular Physiology >GM13133 is a negative regulator in mouse white adipocytes differentiation and drives the characteristics of brown adipocytes
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GM13133 is a negative regulator in mouse white adipocytes differentiation and drives the characteristics of brown adipocytes

机译：GM13133负监管机构在白老鼠脂肪细胞分化和驱动棕色脂肪细胞的特点

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摘要

Obesity is tightly associated with the disturbance of white adipose tissue storing excess energy. Thermogenic adipocytes (brown and beige) exert a critical role of oxidizing nutrients at the high rates through non‐shivering thermogenesis. The recruitment of brown characteristics in white adipocytes, termed browning, has been considered as a promising strategy for treating obesity and associated metabolic complications. Recently, long noncoding RNAs play a crucial role in regulating tissue development and participating in disease pathogenesis, yet their effects on the conversion of white into brown‐like adipocytes and thermogenic function were not totally understood. Here, we identified a mouse brown adipose specific expressed lncRNA, termed GM13133. Moreover, a considerable amount of GM13133 is expressed in adipocytes and actively modulated by cold, β 3 ‐adrenergic agonist and cAMP stimuli, implying a potential role in the conversion from white to brown adipocytes. Overexpression of GM13133 did not affect the proliferation of mouse white pre‐adipocytes, but inhibited white adipocyte differentiation by decreasing lipid accumulation. The forced expression of GM13133 also significantly drove the conversion of white into brown‐like adipocytes with the enhanced mitochondrial biogenesis and the induced expression of brown adipocytes specific markers. A global mRNA analysis further indicated the possible regulatory role of cAMP signaling pathway in GM13133 mediated white‐to‐brown adipocytes conversion. Our results identified a lncRNA‐mediated modulation in primary mouse white adipocyte differentiation and indicate the functional significance of GM13133 in promoting browning of white adipocytes and maintenance of thermogenesis, further providing a potential strategy to treating obesity.
机译：肥胖是紧密相关的干扰白色脂肪组织储存多余的能量。产热的脂肪细胞(布朗和米色)产生氧化在高营养的关键作用利率通过非颤抖生热作用。招聘的棕色白色的特征脂肪细胞,称为褐变,一直在考虑作为一个有前途的治疗肥胖和策略代谢相关的并发症。长非编码rna中发挥至关重要的作用规范组织发展和参与在疾病发病机理,但他们的影响白色转换成棕色脂肪细胞等和产热的功能并不完全理解。脂肪具体表达lncRNA,称为GM13133。GM13133表达在脂肪细胞和积极调制的冷,β3肾上腺素能受体激动剂和营的刺激,这意味着一个潜在的作用转换从白色的棕色脂肪细胞。过度的GM13133没有影响鼠标白提前组织扩散,但是抑制白色脂肪细胞的分化减少脂质积累。GM13133的表达也显著地开车白色转换成棕色的类脂肪细胞增强线粒体生物起源和布朗的诱导表达脂肪细胞特定的标记。分析进一步表明可能的营信号通路的监管作用GM13133白色~还是棕色脂肪细胞介导的转换。lncRNA量调节调制在初级白老鼠脂肪细胞的分化和指示GM13133促进的功能意义布朗宁的白色脂肪细胞和维护生热作用,进一步提供了潜力策略来治疗肥胖症。

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