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Effect of adrenergic blockade on glucagon and growth hormone secretion in normal and diabetic children
Insights
Sympathetic overactivity via alpha receptors may increase growth hormone in diabetic children. Adrenergic blockade did not significantly affect glucagon secretion in normal or diabetic children.
Area of Science:
- Pediatric Endocrinology
- Neuroendocrinology
- Adrenergic Pharmacology
Background:
- Children with diabetes often exhibit altered hormone regulation.
- The role of the sympathetic nervous system in growth hormone and glucagon secretion in pediatric diabetes requires further elucidation.
Purpose of the Study:
- To investigate the impact of alpha and beta adrenergic blockade on basal and arginine-stimulated growth hormone and glucagon secretion in children with and without diabetes.
- To determine if sympathetic overactivity contributes to growth hormone hypersecretion in juvenile diabetes.
Main Methods:
- A study involving normal and diabetic children receiving infusions of arginine alone or with phentolamine (alpha-blockade) or propranolol (beta-blockade).
- Measurements of basal and stimulated growth hormone and glucagon levels were taken.
- Adequacy of blockade was clinically assessed.
Main Results:
- Diabetic children showed a significantly greater peak growth hormone response to arginine compared to normal children.
- Alpha-blockade suppressed the growth hormone response in both groups, while beta-blockade had no significant effect.
- Neither basal nor stimulated glucagon secretion was significantly affected by alpha or beta blockade in either group, despite hyperglycemia in diabetics.
Conclusions:
- Sympathetic overactivity through alpha receptors may play a role in growth hormone hypersecretion observed in juvenile diabetes.
- Neither alpha nor beta adrenergic receptors appear to independently modulate basal or arginine-stimulated glucagon secretion in children.
Abstract:
Studies were conducted in four normal and six diabetic children to assess the role of adrenergic blockade on basal and arginine-stimulated growth hormone and glucagon secreation. Each subject had, on three separate occasions, infusion of arginine alone or in conjunction with alpha (phentolamine) or beta (propranolol) adrenergic blockade. Clinically, there was evidence of adequate blockade by each agent. Basal hormone growth levels were not significantly different in the two groups (1.3 +/- 0.2 to 2.1 +/- 1.0 ng/ml in normal subjects; 3.0 +/- 1.1 to 6.0 +/- 3.1 ng/ml in diabetics (mean +/- 1 SEM)) but the peak growth hormone after arginine was significantly greater in the diabetic children than control subjects (34.3 +/- 7.2 versus 12.3 +/- 3.1); in both groups alpha-blockade suppressed the growth hormone response, whereas beta-blockade had no significant effect. Basal glucagon concentrations were similar in both groups (147 +/- 31 to 214 +/- 21 pg/ml in normal subjects; 100 +/- 20 to 124 +/- 17 pg/ml in diabetics on three different occasions) despite the coexistent hyperglycemia of the diabetics. Neither basal nor maximally stimulated glucagon secretion was significantly affected by alpha or beta blockade in the juvenile diabetic or control children. The results suggest that sympathetic overactivity via alpha receptors may contribute to the hypersecretion of growth hormone in juvenile diabetes and that the alpha or beta adrenergic receptor alone does not appear to modulate basal or arginine stimulated glucagon secretion.