Specific conditions, such as exposure to cold, can induce the production of brown-like adipocytes in white adipose tissue. These adipocytes express high levels of uncoupling protein 1 (UCP1) and energy expended by generating heat. Thus, these are a potential target for the prevention or treatment of obesity. The present study involved a comprehensive analysis of the adipose tissue to understand the relationship between long non-coding RNA (lncRNA) 2310069B03Rik and UCP1. Cold exposure increased both lncRNA 2310069B03Rik and Ucp1 expression in inguinal white adipose tissue (iWAT). However, overexpression of lncRNA 2310069B03Rik suppressed the Ucp1 mRNA expression and the promoter activity of UCP1 in the iWAT primary adipocytes. In addition, compared to the early induction of Ucp1 expression by cold stimulation, the induction of lncRNA 2310069B03Rik expression was later. These results suggest that lncRNA 2310069B03Rik functions as a suppression factor of Ucp1 expression.

中文翻译：

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长的非编码RNA 2310069B03Rik在长时间受冷暴露于鼠类米色脂肪细胞中起Ucp1表达的抑制作用。

特定条件（例如暴露于寒冷）会诱导白色脂肪组织中褐色脂肪细胞的产生。这些脂肪细胞表达高水平的解偶联蛋白1（UCP1），并通过产生热量消耗能量。因此，这些是预防或治疗肥胖症的潜在目标。本研究涉及对脂肪组织的全面分析，以了解长非编码RNA（lncRNA）2310069B03Rik与UCP1之间的关系。冷暴露增加了腹股沟白脂肪组织（iWAT）中的lncRNA 2310069B03Rik和Ucp1表达。但是，lncRNA 2310069B03Rik的过表达抑制了iWAT原代脂肪细胞中Ucp1 mRNA的表达和UCP1的启动子活性。此外，与通过冷刺激早期诱导Ucp1表达相比，稍后诱导lncRNA 2310069B03Rik表达。这些结果表明lncRNA 2310069B03Rik充当Ucp1表达的抑制因子。