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Citation Information: J Clin Invest. 1973;52(10):2468-2485. https://doi.org/10.1172/JCI107438.
Abstract
The concept of an abnormality of glutamine metabolism in primary gout was first proposed on the basis of isotope data: when [15N]glycine was administered to gouty subjects, there was disproportionately great enrichment of N-(3 + 9) of uric acid, which derive from the amide-N of glutamine. An unduly high concentration of 15N in glutamine was postulated, and attributed to a hypothetical defect in catabolism of glutamine. Excess glutamine was proposed as the driving force of uric acid overproduction.
Authors
Oded Sperling, James B. Wyngaarden, C. Frank Starmer
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