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 μmol/liter) and lactate (1222 ± 136 μimol/liter), the main gluconeogenic substrates, were normal and did not correlate with the decrease of hepatic glucose release. Both plasma FFA (552 ± 35 μM) and β-hydroxybutyrate (654 ± 158 μM) 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 < 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.