Effects of Salmon Calcitonin on Insulin-Induced Growth Hormone Release in Man

Abstract

The study was carried out on 6 male volunteers aged 20-44 yr, nonobese, with no clinical evidence of endocrine disorders and free from drug intake. The experiment was performed at 0800 h; the subjects were in a fasting state and resting in bed for 1 h before and throughout the tests. Each subject experienced an insulin tolerance test (0.1 U [unit] of regular insulin i.v./kg body wt. Samples for estimation of blood glucose (enzymatic assay by auto-analyzer) and plasma hGH (human growth hormone, radioimmunoassay) were collected in a basal condition and at 15, 30, 60, 90 and 120 min after insulin administration. The test was repeated after 2 days keeping exactly to the same conditions, except for the addition of 200 U of Salmon Calcitonin (SCT) to the saline containing human albumin 0.1% to prevent its adsorption to glass. Insulin-induced hypoglycemia caused the expected increase in plasma hGH (peak at 30 and 60 min). Infusion of SCT, compared with infusion of saline produced a definite and considerable reduction in the plasma levels of hGH in all 6 subjects tested and at almost all stages. The reduction was highly significant at 30, 60 min (P < 0.001) and at 90, 120 min (P < 0.01). Also the individual and the mean peak values were lower during the infusion of SCT (P < 0.001). As far as insulin-induced hypoglycemia is concerned, a comparison of data obtained during infusion of saline and during infusion of SCT shows no significant blood sugar variations at all stages. The mechanism of the SCT-associated depression of the insulin-induced plasma hGH response is actually unknown: it might be traced to the calcitonin''s action on Ca2+, which within the cells of the anterior lobe of the pituitary might have an intracellular site playing an important part in the synthesis and secretion of hormones. Calcitonin would seem to enhance the inflow of Ca2+ into the mitochondria, the final result being a reduction in the cytoplasmic Ca2+. The fall of cytoplasmic Ca2+ would partly block the activity of the contractile microtubular system dependent on cyclic AMP and Ca2+ and thus reduce the amount of hGH released.