Konjac glucomannan improves hyperuricemia through regulating xanthine oxidase, adenosine deaminase and urate transporters in rats

Abstract

To develop a more effective and safer treatment for Hyperuricemia (HUA), this research investigated the anti-hyperuricemic mechanism of KGM from the perspectives of uric acid (UA) production and excretion in rat model. After four-week experiment, KGM at 168 mg/kg did best in reducing serum UA level. The mechanism of KGM improving HUA was related to its inhibitory capacity to the activities and mRNA expression of xanthine oxidase (XOD) and adenosine deaminase (ADA) in liver. Meanwhile, KGM could also down-regulate the protein expression of uric acid transporters1 (URAT1) and up-regulate the mRNA and protein expression of urate transporter (UAT), organic anion transporter1 (OAT1) and organic anion transporter3 (OAT3) in kidney. Moreover, KGM could also alleviate the renal dysfunction caused by HUA by mitigating urate deposition, and reducing serum creatinine (Cr) and blood urea nitrogen (BUN) levels. KGM might complement existing therapies to improve HUA.

Keywords

• Hyperuricemia
• Konjac glucomannan
• Uric acid
• Xanthine oxidase
• Adenosine deaminase
• Urate transporters