Vine Tea (Ampelopsis grossedentata) Extract Suppresses Postprandial Uric Acid Levels via Both Inhibition of Xanthine Oxidase and Facilitation of Uric Acid Excretion

Abstract

Abstract Objectives This study was aimed to evaluate the effect of vine tea extract (VE) which contained ampelopsin (AMP) on postprandial serum uric acid levels. Methods A randomized, placebo controlled, and crossover study was performed from January 2018 to June 2018. The participants were Japanese male whose fasting serum uric acid levels were between 5.0 mg/dL and 7.0 mg/dL. The purine (RNA) loading test was conducted in this study. In brief, after fasting blood collection, the subjects ingested 4 g of yeast RNA and trial supplements (500 mg of VE (150 mg of AMP) or placebo), their blood and urine were subsequently collected every 1 hr for 4 hr. Uric acid and creatinine (Cr) levels in the blood and urine were measured. The primary outcome was postprandial uric acid area under the curve (AUC) and the secondary outcomes were postprandial uric acid, Cr clearance, urinary uric acid excretion, uric acid clearance, and fractional excretion of uric acid (FEUA). To investigate the urate lowering mechanism of VE, effect of VE or AMP on xanthine oxidase (XO) and urate transporter function was assessed in vitro. Results Of 119 participants screened, 36 males who met inclusion criteria were enrolled and the subjects were randomly assigned to two groups. Of these, 16 in X group and 18 in Y group were completed of the study. The values were expressed as mean ± SE. The postprandial uric acid AUC of VE (199.14 ± 62.38 mg · min/dL) was lower than that of placebo (214.41 ± 66.91 mg · min/dL), but it was not significant (P = 0.166). On the other hand, intake of VE induced the increase of urinary uric acid excretion (180 min; VE 0.58 ± 0.03 mg/kg/hr; P0.52 ± 0.03 mg/kg/hr; P = 0.044) and FEUA (180 min; VE 0.58 ± 0.03 mg/kg/hr; P 0.52 ± 0.03 mg/kg/hr; P = 0.044). These results suggest VE facilitate the uric acid excretion. An exploratory efficacy analysis was performed on 23 subjects whose eGFR values were less than 89 mL/min. As a result, the intake of VE suppressed postprandial uric acid elevation in those subjects significantly. AMP and VE inhibited the activity of XO in vitro. In addition, AMP weakly inhibited the function of OAT4, one of the urate reabsorption transporters. Conclusions These results suggested that intake of VE inhibited uric acid synthesis and facilitated of urate excretion, thereby suppression of the elevation of postprandial serum uric acid was observed. Funding Sources This study was supported by FANCL Corporation.