脂肪组织能量稳态的失调，是导致肥胖及相关代谢性疾病的重要原因。Klf10属于Kruppel-like factor (Klfs) 转录因子家族成员，其在脂肪组织中的作用尚不明确。我们前期工作发现：1）小鼠脂肪组织中Klf10的表达随着肥胖的发生而上调; 2) 在3T3-L1前脂肪细胞中过表达Klf10，可抑制脂肪细胞分化，而在3T3-L1成熟脂肪细胞中过表达Klf10，可以提高脂肪细胞对胰岛素敏感性；3) 在肥胖小鼠皮下脂肪过表达Klf10，可以抑制脂肪组织炎症、提高小鼠胰岛素敏感性。本项目将基于前期基础，结合细胞/分子生物学实验和肥胖小鼠模型的研究，深入探寻Klf10在调节脂肪细胞分化、脂肪组织能量稳态中的作用及机制。该研究有助于阐明脂肪细胞分化的分子机制，并为防治肥胖及其相关疾病提供新的思路及靶点。

The dysregulation of adipose tissue homeostasis is an important cause for obesity and its related metabolic disorders. Klf10 is belongs to a family of Kruppel-like factor (Klfs) transcriptional factors and little is known about its role in adipose tissue function. In our previous study, we found 1) Adipose tissue Klf10 expression level is increased in obese mice; 2) Overexpression of Klf10 in 3T3-L1 preadipocytes inhibit adipogenesis, while overexpression of Klf10 in 3T3-L1 mature adipocytes increases adipocytes' insulin sensitivity; 3) Adenovirus-mediated overexpression of Klf10 in subcutaneous fat of obese mice inhibits adipose tissue inflammation and improves insulin sensitivity. Based on these results obtained previously, we will combine the experimental methods of cellular/molecular biology and the studies of obese mice models to further investigate the role and mechanism of Klf10 in regulating adipogenesis and adipose tissue homeostasis. These studies may provide new insights into the mechanism of adipogenesis and therapeutic targets for the prevention and treatment of obesity and its related metabolic disorders.