Exploration of glucose homeostasis during fasting in growth hormone‐deficient children

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 Յ2.6 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 ¼ 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. ٖ Fasting, glucagon, hypoglycaemia, ketogenesis D Jaquet, Paediatric Endocrinology and Diabetology Units, Hôpital Robert Debré, 48 Boulevard Serurier,

The impact of fasting and treatment omission on susceptibility to hypoglycaemia in children and adolescents with GH and cortisol insufficiency

“…Children with GH or cortisol deficiency who miss breakfast could exacerbate differences in neurological performance that have been described between them and their peers 23 . BG concentrations were related to age, in contrast to an earlier study in fasting children with hypopituitarism, 21 but it was not just the youngest children who became hypoglycaemic and therefore any advice regarding hypoglycaemia should be given to all patients with PHD.…”

“…Second, neurophysiological changes can be observed in children when BG concentrations are at this level 19 and finally, a counter‐regulatory hormone response was expected when BG concentrations fell to 3·3 mmol/l 17,20 . Jaquert and colleagues 21 studied 10 children with either GHD, GH and TSH deficiency or panhypopituitarism. The authors defined normal BG values as being in the range 3·2–5·2 mmol/l but hypoglycaemia as a BG ≤ 2·6 mmol/l.…”

Juvenile hyposomatotropism in a Somali cat presenting with seizures due to intermittent hypoglycaemia

“…In human medicine, marked fasting hypoglycaemia has been described in conjunction with GH deficiency, especially in children. 6–10 Several theories on the pathomechanisms of hypoglycaemia due to GH deficiency have been proposed. In general, hypoglycaemia can result from decreased glucose production, increased glucose utilisation or a combination of both.…”

Nocturnal hypoglycaemia in ACTH and GH deficient children: role of continuous glucose monitoring

“…Therefore, ascertainment of the effectiveness of replacement therapy in preventing nonsymptomatic hypoglycaemic episodes in ACTH/GH deficient children is crucial for their neurological outcome. Data on this issue are conflicting, some authors reporting multiple hypoglycaemic episodes, others providing reassuring results . The heterogeneity of the study populations (including both isolated and combined ACTH and GH deficiency), the different cut‐off values for defining hypoglycaemia and the use of different methods for recording glucose levels may account for the discrepancies.…”

“…Consequently, children with CAI may have nocturnal hypoglycaemia. This is especially true in children with associated GHD, which represents an additional risk factor for hypoglycaemia …”