Effects of hypopituitarism and growth hormone replacement therapy on the production and utilization of glucose in childhood.

Abstract

Glucose metabolism during fasting was investigated in 10 children aged 1.5 month-11.5 yr with deficiency of GH with or without other pituitary hormone deficiencies. After 10-16 h of fasting, mean plasma glucose was 56 +/- 4 (SEM) mg/dl, the result of decreased hepatic production of glucose (3.3 +/- 0.3 mg kg-1 min-1) insufficient to match glucose utilization (3.6 +/- 0.4 mg kg-1 min-1). The diminution of plasma glucose and of glucose production was similar whether ACTH deficiency was present (3.2 +/- mg kg-1 min-1) or not (3.5 +/- 0.6 mg kg-1 min-1). These results indicate that the lack of GH was the primary cause of hypoglycemia. Fasting plasma alanine (212 +/- 41 mumol/liter) and lactate (1222 +/- 136 mumol/liter), the main gluconeogenic substrates, were normal and did not correlate with the decrease of hepatic glucose release. Both plasma FFA (552 +/- 35 microM) and beta-hydroxybutyrate (654 +/- 158 microM) were in the low normal range, and neither correlated with the rate of glucose utilization. hGH replacement therapy resulted in a normalization of fasting plasma glucose concentration (78.5 +/- 6 mg/dl, P less than 0.005) and hepatic glucose production (6.1 +/- 1.2 mg kg-1 min-1). No significant changes occurred in the plasma concentrations of gluconeogenic or lipid substrates. These results, together with the known stimulatory effects of GH on carbohydrate-induced insulin secretion and storage of hepatic glycogen, suggest that the changes in glucose production in untreated and GH treated patients reflect the degree of hepatic glycogen replenishment.