Allopurinol decreases serum uric acid level and intestinal glucose transporter-5 expression in rats with fructose-induced hyperuricemia

• Allopurinol and benzbromarone both significantly reduce the serum level of uric acid in rats with fructose-induced hyperuricemia.
• Allopurinol, not benzbromarone, lowers intestinal GLUT5 protein expression.
• Both allopurinol and benzbromarone do not affect the intestinal GLUT2 expression.

BackgroundHigh fructose consumption is considered to be related to the increasing prevalence of hyperuricemia (HUA). Glucose transporters (GLUT) 2 and 5 are crucial for fructose absorption and transporter. Effects of anti-HUA drugs, allopurinol (API) and benzbromarone (BBR), on expressions of GLUT5 and GLUT2 are not evaluated.MethodWistar rats were given 10% fructose in drinking water for 60 days to induce HUA, and 5 mg/kg API and 10 mg/kg BBR were intragastricly treated for 30 days. Serum level of uric acid and xanthine oxidase (XOD) activity in liver were determined. Expressions of GLUT2 and GLUT5 in intestine were analyzed by immunohistochemistry staining assay and Western blot assay.ResultsTreatment with API or BBR significantly decreased the serum level of uric acid in HUA rats induced by fructose. Meanwhile, API treatment significantly reduced the XOD activity in liver and GLUT5 expression in intestine. However, BBR treatment did not show inhibitory effects on hepatic XOD activity and intestinal GLUT5 expression. In addition, treatment with API or BBR did not show any effect on GLUT2 expression in intestine.ConclusionAPI decreases serum level of uric acid in fructose-induced HUA rats. The mechanisms are associated with suppressing XOD activity in liver to reduce uric acid production, and inhibiting GLUT5 expression in intestine to reduce fructose absorption.

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