慢性炎症反应在胰岛素抵抗和2型糖尿病的发生发展中发挥重要作用，但机制尚不完全清楚。甲酰肽受体2（FPR2）属于趋化物质受体家族，参与感染及损伤引起的炎症反应和炎症相关疾病，但在胰岛素抵抗和2型糖尿病中的作用尚不清楚。我们预实验发现，小鼠FPR2（mFPR2）表达于脂肪组织、肝脏和骨骼肌；高脂饮食诱导的肥胖小鼠腹部脂肪组织和骨骼肌mFPR2表达升高。利用Fpr2基因敲除小鼠发现 mFPR2缺失能显著改善高脂饮食导致的胰岛素抵抗、高血糖及高胆固醇血症。这些结果提示mFPR2在胰岛素抵抗、高血糖及高胆固醇血症的发生中发挥重要作用。本课题拟进一步通过动物、细胞和分子水平的研究，揭示 mFPR2发挥作用的分子机制。本研究不但能加深我们对胰岛素抵抗和糖脂代谢紊乱机制的了解，而且有可能为治疗2型糖尿病和高胆固醇血症提供新靶标，具有重要的理论意义和潜在的临床价值。

Chronic inflammation plays important roles in the development of insulin resistance and type 2 diabetes, but the underlying mechanisms are poorly understood. Formyl peptide receptor 2 (FPR2) belongs to chemoattractant receptor family. It is involved in infection- and injury-induced inflammatory responses and inflammation related disorders. It’s not clear whether FPR2 contributes to insulin resistance and type 2 diabetes. Our preliminary results showed that mouse FPR2 (mFPR2) is expressed in adipose tissue, liver and skeletal muscle. mFPR2 is elevated in adipose tissue and skeletal muscle in high fat diet-induced metabolic disorder mouse model. Depletion of mFPR2 alleviates high-fat diet induced insulin resistance, hyperglycemia and hypercholesterolemia. These results suggest that mFPR2 plays critical roles in high fat diet-induced dysregulation of glucose and cholesterol metabolism. In this project, we will investigate the contribution of mFPR2 to high-fat diet induced insulin resistance, hyperglycemia and hyperchoelsterolemia and explore the underlying mechanisms. Our study will provide potential therapeutic targets against type 2 diabetes and hypercholesterolemia.