The Role of Growth Hormone and Cortisone on Glucose and Gluconeogenic Substrate Regulation in Fasted Hypopituitary Children

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Abstract
Panhypopituitarism may be associated with spontaneous hypoglycemia and marked insulin sensitivity. Five children with both growth hormone (GH) and adrenocorticotrophin (ACTH) insufficiency were studied in three periods: a) on no therapy; b) during cortisone acetate; and c) during GH and cortisone acetate replacement. With total caloric restriction prior to therapy, all patients became hypoglycemic (109 ± 18 → 37 ± 3.5 mg/dl, mean ± SEM) and ketonemic (β-hydroxybutyrate 0.10 ± 0.02 → 3.04 ± 0.63 mM and acetoacetate 0.05 ± .01 → 0.80 ± 0.15 mM) within 30 hours. Glutamine and alanine concentrations fell with fasting (511 ± 13 → 293 ± 26 μM and 394 ± 58 → 137 ± 12 μM, respectively) but to levels lower than in normal children. However, only alanine was significantly lower (P < 0.05). With cortisone plus GH therapy, fasting glycemia was improved (73 ± 6 mg/dl) at 30 hours fasting and was associated with increased alanine and glutamine concentrations (206 ± 28 μM and 448 ± 40 μM, respectively) and less ketonemia (β-hydroxybutyrate 1.13 ± 0.39 mM). Cortisone therapy alone resulted in intermediate improvement of these values. Only combined therapy resulted in increased lactate and pyruvate concentrations, which fell to normal with fasting. Fasting urinary ammonia excretion was unchanged whereas urea nitrogen excretion decreased significantly with therapy. The responses to alanine infusions following each study period in one patient were normal. The glycemic response to iv glucose was similar during each study period; however, post-prandial and glucose-stimulated insulin responses were increased with cortisone and cortisone plus GH therapy. We suggest that the hypoglycemia observed in hypopituitary patients is a substrate-mediated phenomenon, and that cortisone and growth hormone replacement therapy improve fasting glucose homeostasis, increase circulating alanine and glutamine concentrations, and decrease hepatic gluconeogenesis. These effects may be mediated through an increase in fat catabolism.

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