Abstract
We propose that calcitonin, secreted in response to the intake of food, aids in routing calcium, obtained by intestinal absorption, into bone fluid. Here calcium is temporarily stored in combination with phosphate for return to the extracellular fluid (blood) during intervals between oral intakes of calcium. The net result is a conservation of calcium postprandially and a decrease in parathyroid hormone-induced bone destruction during subsequent fasting periods. Evidence for this postulate is provided in the following six sequential steps from the time a calcium-containing meal is consumed until that portion of calcium stored in bone fluid is utilized during fasting periods to aid in plasma calcium maintenance. (i) Calcitonin secretion is stimulated by feeding and subsequent digestive processes. (ii) Postprandial secretion of calcitonin restricts the efflux of calcium from bone fluid to blood, thereby maintaining parathyroid hormone (PTH) secretion. (iii) In thyroid-intact individuals, both PTH and calcitonin are secreted postprandially and act in concert on calcium homeostasis. (iv) Calcitonin actively moves phosphate into bone and prevents its loss from bone fluid to blood. (v) Postprandial storage of calcium with phosphate occurs in bone fluid of thyroid-intact individuals. (vi) This labile storage form of calcium is the first to be utilized during fasting periods. In the absence of partial disruption of this storage mechanism, rapid development of pathological bone conditions would not be expected because PTH action permits the extended utilization of bone calcium for plasma calcium control. However, augmentation of osteopenic conditions could be expected if long-term low calcium intake were accompanied by a malfunction of this calcitonin-induced system for calcium storage.