肥胖病人易患非酒精性脂肪肝（NAFLD），从脂肪因子的角度理解其原因，可为防治NAFLD提供新视角。脂肪因子Chemerin可以趋化巨噬细胞，在NAFLD病人中高表达，我们前期结果发现Chemerin敲除小鼠更容易高脂诱导脂肪肝，目前Chemerin在NAFLD中的作用没有定论且分子机制未见报道。本课题拟从细胞、动物和人组织标本3个层次研究Chemerin与NAFLD的相关性；在肝细胞脂肪累积模型上探索Chemerin直接调控肝细胞脂代谢以及参与受体和信号通路；在Chemerin以及受体敲除小鼠和过表达Chemerin小鼠中研究Chemerin对肝细胞的直接作用和Chemerin如何影响肝脏枯否细胞（kupffer cell）的极化和肝脏的炎症状态，进而调控NAFLD的发生。通过研究可为深刻理解Chemerin对NAFLD发生的分子机制，为寻找防治NAFLD的分子靶点提供理论基础。

Obesity is a high risk factor for nonalcoholic fatty liver disease (NAFLD).We try to understand why NAFLD is so normal in the obese from the perspective of adipokine. It would be helpful for prevention and treatment of NAFLD. Chemerin is a new adipokine identified in 2007, and is expressed highly in patients with NAFLD. we found that Chemerin knockout mice could be induced NAFLD easily than wide type by high fat diet.The roles of Chemerin in NAFLD is not conclusive and the molecular mechanism has not been reported. We try to find the corelation between Chemerin and NAFLD in cells, animals and human tissues.We will explore the roles of Chemerin on fatty acid metabolism in liver cells, the involving Chemerin receptors and signaling pathways in fatty liver cell models. In Chemerin knockout mice, Chemerin receptor knockout mice and Chemerin overexpression transgenic mice, we will study how Chemerin effect on hepacytes, liver Kupffer cells polarization and inflammation. This study can provide deeply understanding on the molecular mechanism of Chemerin on NAFLD, and provide potential targets for prevention and treatment of NAFLD.