近年代谢综合征的发病率显著增高，但其发病机制迄今尚未完全明了。FAM3家族是2002年克隆的一个细胞因子样家族，我们前期已发表的文章提示FAM3A及PANDER在肝脏糖脂代谢过程中起重要作用，目前国内外尚无关于FAM3C是否参与糖脂代谢调控的报道。本项目的预实验研究发现，FAM3C在db/db及HFD小鼠肝脏中表达降低，肝脏过表达FAM3C后能显著降低db/db小鼠的空腹高血糖、改善糖耐量并缓解脂肪肝；进一步的机制研究提示FAM3C能通过激活Akt减少糖异生及脂肪酸合成。本课题将在预实验研究结果的基础上：1.在db/db小鼠及HFD小鼠肝脏过表达FAM3C，分析FAM3C对糖脂代谢关键基因的影响；2.在细胞水平上对FAM3C参与肝脏糖脂代谢的机制进行深入探讨；3.进一步结合临床脂肪性肝病的发病与FAM3C表达的关系，以期为临床代谢综合征的治疗提供新思路。

In recent years, the incidence of metabolic syndrome was significantly increased, but its pathogenesis is poorly understood. FAM3 gene family is a recently identified cytokine-like gene family in 2002. Our previous published study demonstrated that FAM3A and PANDER play a critical role in regulation of hepatic glucose and lipid metabolism. But there is no report that if FAM3C is involved in the regulation of hepatic glucose and lipid metabolism. Our previous studies have found that FAM3C expression was significantly reduced in the liver of db/db and high-fat diet (HFD)-induced diabetic mice. Hepatic FAM3C overexpression markedly attenuated hyperglycemia and fatty liver in diabetic mouse models. Further study found that FAM3C through activation of Akt to reduce gluconeogenesis and fatty acid synthesis. In this research project, based on our previous study, we further analysis the key gene in glucose and lipid metabolism in db/db mice and HFD mice liver after FAM3C overexpression; and investigate the mechanism of FAM3C involved in glucose and lipid metabolism in vitro; then compare the incidence of clinical fatty liver disease with the expression level of FAM3C in human liver, in order to provide some new ideas for the clinical treatment of metabolic syndrome.