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U.S. Department of Agriculture/ARS Western Human Nutrition Research Center, University of California at Davis, Davis, CA 95616;
* U.S. Department of Agriculture/ARS Arkansas Children’s Nutrition Center, Little Rock, AR 72202; and
Department of Pomology, University of California, Davis, CA 95616
3To whom correspondence should be addressed. E-mail: rjacob{at}whnrc.usda.gov.
To assess the physiologic effects of cherry consumption, we measured plasma urate, antioxidant and inflammatory markers in 10 healthy women who consumed Bing sweet cherries. The women, age 22–40 y, consumed two servings (280 g) of cherries after an overnight fast. Blood and urine samples were taken before the cherry dose, and at 1.5, 3 and 5 h postdose. Plasma urate decreased 5 h postdose, mean ± SEM = 183 ± 15 µmol/L compared with predose baseline of 214 ± 13 µmol/L (P < 0.05). Urinary urate increased postdose, with peak excretion of 350 ± 33 µmol/mmol creatinine 3 h postdose compared with 202 ± 13 at baseline (P < 0.01). Plasma C-reactive protein (CRP) and nitric oxide (NO) concentrations had decreased marginally 3 h postdose (P < 0.1), whereas plasma albumin and tumor necrosis factor-
were unchanged. The vitamin C content of the cherries was solely as dehydroascorbic acid, but postdose increases in plasma ascorbic acid indicated that dehydroascorbic acid in fruits is bioavailable as vitamin C. The decrease in plasma urate after cherry consumption supports the reputed anti-gout efficacy of cherries. The trend toward decreased inflammatory indices (CRP and NO) adds to the in vitro evidence that compounds in cherries may inhibit inflammatory pathways.
KEY WORDS: • cherries • gout • humans • anti-inflammatory • fruit
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