Effect of renal transporter Glut9 on hyperuricemia in rats induced by fructose

AIM: To explore the effect of renal transporter glucose transporter 9 (Glu9) on hyperuricemia in the rats induced by fructose.METHODS: SD male rats (n=30) were randomly divided into normal group, model group and benzbromarone group, according to the weight. The rats in normal group was given water, while the rats in model group and benzbromarone group were given 10% fructose solution to establish hyperuricemia model. At the same time, the rats in normal group and model group were given a gavage of distilled water, while the rats in benzbromarone group were given benzbromarone at the dose of 20 mg/kg. The rats were sacrificed on the 40th day. The serum uric acid (SUA) and urinary uric acid (UUA) were detected to calculate the clearance rate of uric acid (CUA) in the kidney. The activity of hepatic xanthine oxidase (XOD) was also measured. The expression of renal Glut9 at mRNA and protein levels was determined by RT-qPCR and immunohistochemical staining. RESULTS: From the 20th day to the 40th day, the SUA in model group was significantly higher than that in normal group, but the UUA and CUA had no difference. On the 20th day, the SUA in benzbromarone group was markedly decreased as compared with model group, but UUA and CUA had no significant difference. On the 40th day, the hepatic XOD activity in model group was significantly elevated, and no difference of XOD between model group and the benzbromarone group was observed. Compared with normal group, the protein expression of Glut9 in the renal tissues of model group were markedly increased, and that in benzbromarone group was significantly lower than that in model group. However, no difference of the Glut9 mRNA expression was observed among groups. CONCLUSION: Fructose drinking induces hyperuricemia in rats, which is probably related to the up-regulation of renal Glut9 expression at protein level, and the increase in the reabsorption of uric acid in the kidneys.