THE ENZYME glucose-6-phosphate dehydrogenase (G6PD) initiates the oxidative decarboxylation of glucose-6-phosphate in the pentose phosphate pathway. This reaction results in the regeneration of the coenzyme TPNH, and the formation of CO2 and pentose phosphate.
Since G6PD is present in most human tissues,1 the question whether abnormalities in glucose metabolism exist in patients with G6PD deficiency is raised.
Isotopic studies measuring the rate of glucose oxidation by the whole body from both glucose-1-C14 and glucose-6-C14 have demonstrated markedly diminished C14O2 in the expired air of G6PD deficient males.2
An abnormal oral glucose tolerance response in G6PD deficient subjects, suggesting a diabetic tendency, was reported by Chanmugam and Frumin.3 Pointing out that diabetic state is usually mild, occurring later in life, and may be relatively asymptomatic, these authors stated that it is still unknown whether similar results would be obtained with children possessing