Subject(s)
Humans , Male , Infant , Glycogen Storage Disease/complications , Glycogen Storage Disease/diagnosis , Glycogen Storage Disease/drug therapy , Adrenal Cortex Hormones/therapeutic use , Lung Diseases, Interstitial/complications , Lung Diseases, Interstitial/diagnosis , Lung Diseases, Interstitial/drug therapy , Heart Defects, Congenital/complications , Heart Defects, Congenital/diagnosisABSTRACT
Paradoxically, ethanol, which raises lactate in normal individuals, lowers the elevated levels of lactate in patients with Type I glycogenosis. We found that, although lactate levels fell, pyruvate proportionately declined even more, resulting in an increased L/P ratio which indicates that, as in the normal, the oxidation of ethanol had generated NADH. In type I glycogenosis, the increased level of pyruvate-lactate derives from glycogenolysis. We found that, despite continued glycogenolysis, ethanol had caused less pyruvate-lactate to form. The effect of an increased NADH/NAD+ ratio on the flow of carbon through the Embden-Meyerhof pathway could account for the finding, presumably by its effect on the oxidation-reduction couples with diversion of carbon toward formation of triglyceride rather than pyruvate-lactate.