Abstract

The purpose of this study was to investigate the preventive effects of fucoidan (Fc) and fucoxanthin (Fx) on hyperuricemic rats. Sprague Dawley (SD) rats were randomly assigned to seven groups: a control group, a hyperuricemia (HUA) group, low- and high-dose Fx groups, a Fc group, a combination Fc and Fx group, and a positive control group. Three weeks after the interventions, each group was given potassium oxonate (PO) and hypoxanthine (HX) to induce HUA in all groups except for the control group, and the rats were then sacrificed. Blood and urine were analyzed for biochemical properties, and differences in urine volume were determined. Livers and kidneys were collected to analyze xanthine oxidase (XO) activity and the expression of uric acid (UA) transporter-related proteins (GLUT9, ABCG2, OAT1, URAT1). The results show that HUA was successfully induced by PO/HX after 4 h of administration. The activity of XO was significantly reduced by a combination of Fc and Fx. In the combination group, both ABCG2 and OAT1 increased significantly, whereas GLUT9 and URAT1 decreased significantly. In summary, the combination of Fc and Fx can inhibit the activity of XO in the liver and regulate the expression of proteins related to UA transporter in the kidney to reduce the UA level in serum.

Highlights

  • Hyperglycemia, hyperlipidemia, and hypertension are currently the top three major chronic diseases in Taiwan

  • The results showed that the uric acid level was increased at 4, 6, and 9 h after induction

  • The results showed that there was no significant difference in blood urea nitrogen (BUN) between the groups, except for the positive control group compared with the vehicle group (Figure 3B)

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Summary

Introduction

Hyperglycemia, hyperlipidemia, and hypertension are currently the top three major chronic diseases in Taiwan. According to the Nutrition and Health Survey in Taiwan (NAHSIT) data from 2005 to 2008, the prevalence of hyperuricemia (HUA) in Taiwan has increased each year. Hyperuricemia has gradually become the fourth most prevalent chronic disease [1]. High uric acid (UA) concentrations in the body that persist for a long time can increase the risk of gout, cardiovascular disease, kidney-related diseases, diabetes, hypertension, and hyperlipidemia. The current treatment of hyperuricemia is based on pharmaceutical intervention, which is supplemented by changes in diet and lifestyle. Long-term use of medication to lower uric acid levels may cause severe allergic reactions, kidney injury, and even death [2]

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