果糖诱导高尿酸血症大鼠肾脏转运蛋白Glut9研究

IM: To explore the pathological mechanism of hyperuricemia rats induced by fructose from the aspects of renal transporter Glut9. METHODS: Twenty SD male rats were randomly divided into two groups by weight. The normal group was given water, the model group was given 10% fructose water to establish hyperuricemia model. At the same time, all groups were fed with normal feed. The rats were sacrificed on the 40th day. We detected serum uric acid(SUA) and urinary uric acid(UUA) to calculate the clearance rate of uric acid in renal(CUA). The activity of hepatic xanthine oxidase(XOD) was need to be tested. Meanwhile, we examined the expression level of renal transporter Glut9 mRNA using real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) method. RESULTS: From the 10th to the 40th experimental days, the SUA of the model group raised significantly than the normal group, but the CUA and XOD activity of renal had no difference. On the 40th day, the expression level of protein and gene of Glut9 in the renal of model group were higher than that in the normal group. CONCLUSION: Fructose drinking can induce hyperuricemia in rats, which is probably related to the up-regulation of the expression level of protein and gene of renal Glut9 ,and the increase of reabsorption of renal.