Thyrocalcitonin and its role in calcium regulation in mammals

The discovery of thyrocalcitonin, the hypocalcemic, hypophosphatemic hormone secreted by the mammalian thyroid gland, and its current status with respect to cell of origin, chemistry, site and mode of action, and control of its secretion are reviewed. The physiological function of thyrocalcitonin has yet to be established with certainty. Evidence that secretion of thyrocalcitonin prevents postprandial hypercalcemia is presented. Small amounts of calcium administered orally caused hypercalcemia in acutely thyroidectomized but not in intact rats. In the pig, a direct relationship has been established between thyrocalcitonin secretion and levels of blood calcium during hypercalcemia. However, in other studies in which calcium was given orally, thyrocalcitonin secretion rose even without a detectable increase in the concentration of blood calcium. These observations in rats and pigs raised questions regarding the stimulus to the thyroid gland for thyrocalcitonin secretion. Is a small and undetectable rise in the blood calcium after oral calcium a sufficient signal to the thyroid gland or are other factors involved? The recent finding that pentagastrin administered i.v. at low doses increased thyrocalcitonin secretion in pigs suggests that release of gastrin or a related gastrointestinal hormone after oral calcium may thereby aid in regulation of calcium metabolism. The possibility also remains that the principal physiological function of thyrocalcitonin may be unrelated to calcium homeostasis. Attention has been focused on calcium partly because of the nature of the experiments leading to the discovery of thyrocalcitonin. Perhaps the correct pathway to elucidate the true role of this hormone in the body economy has not yet been followed.