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Exploration of glucose homeostasis during fasting in growth hormone-deficient children
Insights
Growth hormone (GH)-deficient children exhibit a high risk of hypoglycemia during fasting. This may stem from insufficient ketogenesis or impaired glycogenolysis, impacting glucose homeostasis.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Glucose Homeostasis
Background:
- Growth hormone (GH) deficiency is associated with metabolic disturbances.
- The precise risk of hypoglycemia and the role of GH in glucose regulation in these children require further elucidation.
Purpose of the Study:
- To assess the risk of hypoglycemia in GH-deficient children during a 24-hour fast.
- To investigate the underlying mechanisms contributing to hypoglycemia in this population.
Main Methods:
- A 24-hour fasting study was conducted on 10 children with GH deficiency (aged 1.1-6.5 years).
- Blood glucose, lactate, pyruvate, and ketone bodies were monitored.
- Glucagon stimulation tests were performed to assess hepatic glycogen response.
Main Results:
- 90% of GH-deficient children experienced asymptomatic hypoglycemia (blood glucose ≤ 2.6 mmol/l).
- Plasma ketone body levels were lower than expected, suggesting insufficient ketogenesis.
- Normal hepatic glycogen content was indicated by glucagon response, but impaired glycogenolysis was suspected.
Conclusions:
- GH-deficient children have a significant tendency towards hypoglycemia, even beyond infancy.
- Hypoglycemia in these children may result from insufficient ketogenesis and/or a defect in glycogenolysis.
- Further studies are needed to confirm these findings and explore metabolic changes during fasting.
Abstract:
In order to define more precisely the risk of hypoglycaemia in GH-deficient children and to clarify the role of growth hormone (GH) in glucose homeostasis, a 24-h fast was monitored in 10 GH-deficient children aged 1.1-6.5 y. Asymptomatic hypoglycaemia (blood glucose < or = 2.6 mmol/l) occurred in 9/10 children, 2 of whom prematurely interrupted the test. Blood glucose profile was not reproducible between children and had no correlation with age (p = 0.48). Gluconeogenesis was considered as non-altered as read from the normal plasma lactate 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 insufficient ketogenesis which could exacerbate hypoglycaemia in GH-deficient children if brain glucose utilization were not alleviated by ketone body 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 the prolonged fast and its concomitant hypoglycaemia, and would therefore tend to suggest a defect in glycogenolysis. These results confirm the tendency to hypoglycaemia, even after infancy, in GH-deficient children. These hypoglycaemias may occur by different types of malfunctioning, such as insufficient ketogenesis or a defect in glycogenolysis. These hypotheses require confirmation by a more systematic study of the metabolic and hormonal changes that occur during fasting in both GH-deficient and normal children.