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P. F. BOUGNÈRES, P. FERRÉ, J. L. CHAUSSAIN, J. C. JOB, Glucose Metabolism in Hyperinsulinemic Infants: the Effects of Fasting and Sodium dl-β-Hydroxybutyrate on Glucose Production and Utilization Rates, The Journal of Clinical Endocrinology & Metabolism, Volume 57, Issue 5, 1 November 1983, Pages 1054–1060, https://doi.org/10.1210/jcem-57-5-1054
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Glucose metabolism was investigated in four infants aged 3–32 months with persistent hypoglycemia and hyperinsulinism of neonatal onset. Fasting hypoglycemia was found to be due both to an insulin-induced decrease in hepatic glucose output to 3.95 ± 0.30 (sem) mg/kg·min, a value about two thirds of normal, and to a glucose utilization rate of 4.25 ± 0.32 mg/kg·min, which exceeded glucose production by about 8%. Simultaneously, and despite hypoglycemia, fasting plasma d-β-hydroxybutyric acid concentrations were inappropriately low: 406 ± 146 μm, presumably the result of elevated circulating insulin levels.
The infusion of sodium dl-β-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 μm, P < 0.005), without detectable changes in insulin secretion estimated from circulating C-peptide values. Unepxectedly, the increase of plasma glucose was due. to the restoration of glucose production up to 6.7 ± 0.2 mg/kg·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.
