SummaryFactors which may explain lower serum uric acid in a new therapy of patients with glycogen storage disease (GSD) type I have been studied. [1-14C]Glycine incorporation into urine uric acid was 0.68% of the injected dose during a 6-day period of frequent high carbohydrate feedings, 0.40% with the same diet and nocturnal nasogastric feeding by Vivonex, and 0.18% in a control patient with GSD type III. Fractional renal uric acid excretion in the patient with GSD type I increased from 11.3% to 26.3% after beginning nocturnal nasogastric feeding of Vivonex. Red cell phosphoribosylpyrophosphate levels were not changed by the therapy. Addition of Vivonex nocturnal feedings to frequent high carbohydrate feedings (1) decreased the accelerated de novo purine synthesis to a level still higher than control and (2) increased fractional renal uric acid excretion.SpeculationNear normalization of purine metabolism with nocturnal feeding should decrease the risk of gout in GSD type I.