Studies of insulin secretion in infantile hypoglycemia

Abstract

Studies were carried out to evaluate insulin secretion and its suppressability by epinephrine in 6 infants with severe fasting hypoglycemia prolonged into the first year of life. All infants required constant glucose infusions to maintain blood glucose above 40mg%. Decreased hepatic glucose output was responsible for the hypoglycemia in two of the infants (one with isolated ACTH deficiency and one with fructose-1,6-diphosphatase deficiency), whereas increased peripheral utilization of glucose was causative in the remaining four infants (two with islet cell hyperplasia and two with insulinoma). In all cases the rate of glucose infusion was adjusted to produce a peripheral blood glucose of 80 to 100 mg%. The infants with reduced hepatic glucose output had significantly slower rates of glucose infusion and significantly lower plasma insulin concentrations. The infants were next infused with the same amounts of glucose containing epinephrine and propanolol for one hour. Epinephrine completely suppressed plasma insulin (to levels of <12uU/ml) in the infants with decreased hepatic glucose output and beta cell hyperplasia, but had little or no effect on insulin concentrations in the two infants with insulinoma. In all cases the efficacy of propanolol blockade was attested to by the absence of any change in plasma free fatty acid concentrations. Islet cell hyperplasia may be distinguished from insulinoma preoperatively in this way.

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