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


METHODS
Wistar rats were given 10% fructose in drinking water for 60 days to induce HUA, and 5mg/kg API and 10mg/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.


RESULTS
Treatment 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.


CONCLUSIONS
API 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.
Chongqing Key Laboratory of Nature Medicine Research, College of Environment and Resources, Chongqing Technology and Business University, Chongqing, China; Chongqing Key Lab of Catalysis and Functional Organic Molecules, College of Environment and Resource, Chongqing Technology and Business University, Chongqing, China. Electronic address: gangch_tcm@163.com.
Gang
G
Chen
Department of Combination of Chinese and Western Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ping
P
Jia
D000493:Allopurinol / Q000494:pharmacology*; D000818:Animals; D001553:Benzbromarone / Q000494:pharmacology; D005632:Fructose; D051273:Glucose Transporter Type 2 / Q000096:biosynthesis; D051296:Glucose Transporter Type 5 / Q000096:biosynthesis*; D033461:Hyperuricemia / Q000097:blood / Q000139:chemically induced / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008297:Male; D051381:Rats; D014527:Uric Acid / Q000097:blood*; D014969:Xanthine Oxidase / Q000378:metabolism
D051273:Glucose Transporter Type 2; D051296:Glucose Transporter Type 5; D014527:Uric Acid; D005632:Fructose; D001553:Benzbromarone; D000493:Allopurinol; D014969:Xanthine Oxidase
Allopurinol; Benzbromarone; Fructose; Glucose transporters; Hyperuricemia