肥胖发生与白色脂肪过度分化和棕色脂肪缺乏密切相关。非编码RNA参与白色脂肪分化以及棕色化过程，但tRNA衍生的小RNA（tsRNA）相关研究至今未见报道。在前国自然资助下发现，小鼠在冷刺激等手段处理后，棕色脂肪组织被激活。皮下白色脂肪组织中高表达UCP1，并呈现棕色化特征，同时tsRNA呈规律性差异分布，tRFVal上调后使糖皮质激素活化酶（11β-HSD1）被抑制，tRFGly下调使PGC1α被激活。据此提出假说：在冷刺激等处理下，tsRNA一面通过下调糖皮质激素水平调控脂肪细胞生长分化，一面激活PGC1α通路，启动白色脂肪组织棕色化进程，增加耗能，缓解肥胖。本课题拟利用小鼠和细胞模型，应用过表达和RNA干扰等技术手段，从分子、细胞、动物等多层次明确其在脂肪细胞分化中的作用，阐明其在白色脂肪棕色化过程中的作用机制。本课题将从白色脂肪棕色化新视角探讨肥胖的发生机制，为肥胖防治提供新思路。

Obesity is closely related to white fat over-differentiation and brown fat deficiency. Non-coding RNA is involved in white adipose differentiation and browning, but tRNA-derived small RNAs (tsRNA) related studies have not been reported so far. Funded by the last National Natural Science Foundation of China (81471071), brown adipose tissue was activated after treatment with cold stimulation. UCP1 was highly expressed in subcutaneous white adipose tissue and showed browning characteristics. At the same time, tsRNA showed a regular differential distribution. After upregulation of tRFVal, glucocorticoid activating enzyme (11β-HSD1) was inhibited, and tRFGly was down-regulated to activate PGC1α. Based on this hypothesis: under the treatment of cold stimulation, tsRNA regulates the growth and differentiation of adipocytes by down-regulating the level of glucocorticoids, and activates the PGC1α pathway to initiate the browning process of white adipose tissue, increasing energy consumption and alleviating obesity. This project intends to use mouse and cell models, using techniques such as overexpression and RNA interference, to clarify its role in adipocyte differentiation from molecular, cellular, and animal levels, and to elucidate its role and regulatory mechanism in the process of white fat browning. This topic will explore the mechanism of obesity from a new perspective of white fat browning, and provide new ideas for obesity prevention.