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NORMAL, PRODUCTION AND INCREASED OXIDATION OF GLUCOSE ASSOCIATED WITH EPINEPHRINE DEFICIENCY IN “KETOTIC” HYPOGLYCEMIA

Neither the current hypothesis that “ketotic” hypoglycemia results from deficient gluconeogenesis nor the alternative of increased glucose oxidation has been adequately tested. Three affected children (H) were compared with their unaffected identical twins (C) while fasting until hypoglycemic or nearly glycogen depleted. Plasma glucose production (flux, measured by constant infusion of 13C-glucose) was the same earlier in the fast during glycogenolysis (H = 19, C = 19 μmoles/min/kg), as well as later when it was derived almost entirely from gluconeogenesis (H = 15, C = 16 μmoles/min/kg). Potentially available glycerol or amino acids for gluconeogenesis (determined from respiratory calorimetry and N excretion) were not less in H (alanine was lower). However, glucose oxidation (by calorimetry) was greater in H while glucose fell rapidly preceding symptoms (H = 17, C = 8 μmoles/min/kg). Urine epinephrine rose in C as glucose fell, but not in H until after becoming hypoglycemic and the maximum was much less (H = 0.6, C = 1.6 ng/min/kg). There was also a delayed rise in plasma lipolysis products and failure to suppress insulin in H. Inhibition of glyoolysis by infusion of 2-deoxyglucose raised epinephrine, glucose, and FFA in C, but not in H. In conclusion, acquired epinephrine deficiency can account for this impaired transition from glucose bo fat oxidation resulting in hypoglycemia.