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Sympatho-adrenal response to hypoglycaemia in infants
B Stanek1, A Lischka, H Hörtnagl
12nd Department of Internal Medicine, University of Vienna, Austria.
Insights
Hypoglycemia in infants activates the sympathoadrenal system, primarily releasing noradrenaline, unlike adults. This suggests noradrenaline plays a key role in infant glucose regulation.
Area of Science:
- Pediatric Endocrinology
- Neonatal Physiology
- Neuroendocrinology
Background:
- Hypoglycemia, or low blood sugar, poses significant risks in infants.
- The sympathoadrenal system's response to hypoglycemia varies with etiology and age.
- Understanding infant counter-regulatory mechanisms is crucial for managing metabolic disorders.
Purpose of the Study:
- To investigate the sympathoadrenal system's response to hypoglycemia in infants.
- To compare catecholamine release patterns in response to different causes of hypoglycemia.
- To explore the role of noradrenaline in infant glucose homeostasis.
Main Methods:
- Studied seven infants (10-189 days old) with hypoglycemia from various causes.
- Measured plasma noradrenaline and adrenaline levels.
- Monitored heart rate and blood pressure.
Main Results:
- Sympathoadrenal activation occurred in hyperinsulinism and sepsis-induced hypoglycemia, with preferential noradrenaline release.
- Infants with congenital hormone deficiencies showed no sympathoadrenal activation.
- Noradrenaline levels significantly increased in hyperinsulinism and sepsis, unlike adrenaline in some cases.
Conclusions:
- Hypoglycemia activates the infant sympathoadrenal system, with noradrenaline being the primary catecholamine released.
- This contrasts with adult responses and highlights noradrenaline's critical role in infant glucose counter-regulation.
- The findings are significant for understanding and managing infant hypoglycemia.
Abstract:
The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.