ATP结合盒转运蛋白G2（ABCG2）功能异常导致肠道尿酸排泄障碍是高尿酸血症的一个重要原因。法尼酯X受体（FXR）参与了胆汁酸、脂质以及糖类的代谢调控，而在高尿酸血症中的作用尚未明确。前期研究发现：FXR敲除小鼠血尿酸水平升高；FXR可降低高尿酸血症小鼠血尿酸水平，促进肠道ABCG2表达；高尿酸血症患者肠道组织FXR表达明显降低，与ABCG2表达呈正相关；进一步研究发现ABCG2启动子区可能存在FXR潜在的结合位点。在这里我们假设FXR通过增加肠道ABCG2表达促进肠道尿酸的排泌发挥降尿酸作用。本研究拟在体内动物水平探讨FXR降尿酸作用及可能机制；在体外细胞水平研究FXR调控ABCG2表达的分子机制；在临床水平评估FXR与ABCG2表达相关性。本研究不仅能够进一步阐明FXR降尿酸的机制，为其临床应用提供理论依据，更为未来降尿酸治疗提供新的思路。

The decreased intestinal urate excretion caused by ATP-binding cassette transporter,subfamily G,member 2（ABCG2） dysfunction is a common mechanism in hyperuricemia. Farnesoid X receptor (FXR) is involved in the metabolic regulation of bile acids, lipids and carbohydrates, but its role in hyperuricemia has not been clarified. Our Previous experiments showed that the serum uric acid level increased in FXR knockout mice; FXR agonist GW4064 can prevent hyperuricemia and promote intestinal ABCG2 expression; FXR and ABCG2 expression were significantly decreased in the intestinal of hyperuricemia patients, and positively correlated with each other. Further study demonstrated that there might have potential FXR binding sites in ABCG2 promoter region. Here, we propose a hypothesis that FXR can induce ABCG2 expression in transcriptional level, and exerting anti-hyperuricemia effect by promoting intestinal uric acid excretion. We aim to use FXR knockout mice and hyperuricemia models to explore the anti-hyperuricemia effect of FXR and it’s possible mechanism ; Using in vitro study, we try to investigate the potential role of FXR in regulating ABCG2 expression; We attempt to evaluate correction between FXR and ABCG2 expression as well as the clinical significance in human intestinal tissues. This study can elucidate the anti-hyperuricemia effect of FXR, and also provide novel insight into the treatment of hyperuricenmia.