Insulin-induced hypoglycaemia stimulates secretion of parathyroid hormone.
In-vitro and in-vivo studies have suggested a role for the adrenergic system in the regulation of secretion of parathyroid hormone (PTH). In the present study the effects of insulin induced hypoglycaemia on serum concentrations of PTH, cortisol, calcium and phosphate were evaluated in ten healthy subjects. Maximum hypoglycaemia occurred 25 to 35 min after administration of insulin at a standard dose of 0.15 U/kg body weight. All this time there was a slight and transient increase of the serum calcium concentrations whereas there was a marked drop in the serum phosphate levels with a nadir 15 min after maximum hypoglycaemia. Cortisol levels were below baseline when blood glucose was as lowest but increased to a maximum level of 200% 60 minutes after maximum hypoglycaemia. Serum PTH levels increased significantly and reached a maximum of 130% of baseline values concomitant with maximum hypoglycaemia, whereafter they returned to pre-insulin-injection levels within 15 minutes. These findings indicate that during stress endogenous catecholamines affect the secretion of PTH which could be of physiologic importance. In five patients with primary hyperparathyroidism there was, however, no increase in the PTH levels, although they displayed the same response to hypoglycaemia for cortisol and phosphate. This supports previous suggestions that these patients have an impaired capacity to respond to circulating catecholamines.
D000328:Adult; D002118:Calcium / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000097:blood*; D007328:Insulin; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood*; D010710:Phosphates / Q000097:blood
D007328:Insulin; D010281:Parathyroid Hormone; D010710:Phosphates; D002118:Calcium; D006854:Hydrocortisone