Glucose Metabolism in Hyperinsulinemic Infants: the Effects of Fasting and Sodiumdl-β-Hydroxybutyrate on Glucose Production and Utilization Rates

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Abstract
Glucose metabolism was investigated in 4 infants aged 3-32 mo. with persistent hypoglycemia and hyperinsulinism of neonatal onset. Fasting hypoglycemia was due both to an insulin-induced decrease in hepatic glucose output to 3.95 .+-. 0.30 [standard error of the mean] mg/kg .cntdot. min, a value .apprx. 2/3 of normal, and to a glucose utilization rate of 4.25 .+-. 0.32 mg/kg .cntdot. min, which exceeded glucose production by 8%. Simultaneously, and despite hypoglycemia, fasting plasma D-.beta.-hydroxybutyric acid concentrations were inappropriately low; 406 .+-. 146 .mu.M, presumably the result of elevated circulating insulin levels. The infusion of sodium DL-.beta.-hydroxybutyrate resulted in an increase of plasma glucose (48 .+-. 7 vs. 32 .+-. 7 mg/dl, P < 0.01) and lactate (1704 .+-. 217 vs. 964 .+-. 149 .mu.M, P < 0.005), without detectable changes in insulin secretion estimated from circulating C-peptide values. Unexpectedly, the increase of plasma glucose was due to the restoration of glucose production up to 6.7 .+-. 0.2 mg/kg .cntdot. min. The individual increments of plasma lactate and glucose production rate were linearly correlated (P < 0.01). These results together with the known inhibitory effect of ketone bodies on pyruvate dehydrogenation, suggest both increased production of lactate from peripheral recycling of glucose carbon and an increased conversion of this gluconeogenic precursor into glucose.