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The Kinetics of Intramolecular Distribution of 15N in Uric Acid Following Administration of 15N-Glycine: Preferential Labeling of N−(3+9) of Uric Acid in Primary Gout and a Reappraisal of the “Glutamine Hypothesis”

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 41))

Abstract

Patients with primary gout and excessive uric acid excretion fed a test dose of 15N-glycine incorporate increased quantities of 15N into urinary urate [1–4]. Although enrichment of all 4 nitrogen atoms of uric acid is excessive [4,5] that of N−(3+9) is disproportionately great, especially in flamboyant overexcretors of uric acid [5]. Since N−3 and N−9 of uric acid are derived from the amide-N of glutamine [6,7], Gutman and Yu [5,8] proposed a defect in glutamine metabolism in primary gout. Since urinary ammonium, which arises principally from glutamine [9,10], is reduced in many gouty subjects [11,12], they further postulated a reduction of glutaminase activity [5,8]. The hyperglutamatemia of gout has now suggested a defect of glutamate metabolism, with diversion of glutamic acid toward glutamine and purine biosynthesis [13,14].

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Sperling, O., Wyngaarden, J.B., Starmer, C.F. (1974). The Kinetics of Intramolecular Distribution of 15N in Uric Acid Following Administration of 15N-Glycine: Preferential Labeling of N−(3+9) of Uric Acid in Primary Gout and a Reappraisal of the “Glutamine Hypothesis”. In: Sperling, O., De Vries, A., Wyngaarden, J.B. (eds) Purine Metabolism in Man. Advances in Experimental Medicine and Biology, vol 41. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-1433-3_1

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