EXPLORATION OF GLUCOSE-HOMEOSTASIS DURING FASTING IN GROWTH HORMONE-DEFICIENT CHILDREN

In order to define more precisely the risk of hypoglycaemia in GH-defi cient children and to clarify the role of growth hormone (GH) in gluco se homeostasis, a 24-h fast was monitored in 10 GH-deficient children aged 1.1-6.5 y. Asymptomatic hypoglycaemia (blood glucose less than or equal to 2.6 mmol/l) occurred in 9/10 children, 2 of whom prematurely interrupted the test. Blood glucose profile was not reproducible betw een children and had no correlation with age (p = 0.48). Gluconeogenes is was considered as non-altered as read from the normal plasma lactat e and pyruvate concentrations throughout the test. Plasma ketone body concentrations increased during the test, but were lower than expected with respect to the decrease of blood glucose. This suggests insuffic ient ketogenesis which could exacerbate hypoglycaemia in GH-deficient children if brain glucose utilization were not alleviated by ketone bo dy oxidization, as is normally the case. The positive glucose response after glucagon stimulation in 6/10 patients indicated normal hepatic glycogen content. However, these responses were unexpected following t he prolonged fast and its concomitant hypoglycaemia, and would therefo re tend to suggest a defect in glycogenolysis. These results confirm t he tendency to hypoglycaemia, even after infancy, in GH-deficient chil dren. These hypoglycaemias may occur by different types of malfunction ing, such as insufficient ketogenesis or a defect in glycogenolysis. T hese hypotheses require confirmation by a more systematic study of the metabolic and hormonal changes that occur during fasting in both GH-d eficient and normal children.