Stimulation of the secretion of parathyroid hormone during hypoglycemic stress.
The effect and the mechanism of insulin-induced hypoglycemic stress on parathyroid hormone (PTH) secretion in man was evaluated. Porcine crystalline insulin (0.1 U/kg,iv) caused symtomatic hypoglycemia in all subjects. The maximum hypoglycemia occurred between 25 and 35 min following the insulin administration. A significant increase in the serum PTH concentration occurred promptly at 5 min following the time of maximum hypoglycemia, achieving peak levels between 5 and 15 min. Thereafter the serum PTH concentration gradually declined, reaching baseline values of 60 min. Serum cortisol levels were increased, but not until 30 min following the maximum hypoglycemia, and remained significantly elevated at 60 min. Therefore the stimulation of PTH secretion was not caused by elevated levels of serum cortisol. The serum calcium and magnesium levels remained unchanged throughout the procedure. A significant and sustained decline in the serum inorganic phosphate levels occurred following insulin administration. The results indicate that hypoglycemic stress stimulates PTH secretion, presumably via increased epinephrine levels, and further suggest that adrenergic stimuli play an important role in the physiology of PTH secretion.
D000328:Adult; D001786:Blood Glucose; D002118:Calcium / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000139:chemically induced / Q000503:physiopathology*; D007328:Insulin; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood*; D010710:Phosphates / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D010281:Parathyroid Hormone; D010710:Phosphates; D002118:Calcium; D006854:Hydrocortisone