Evidence for an important physiological role for calcitonin

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Abstract
Calcitonin [CT], secreted in response to the intake of food, aids in routing Ca, obtained by intestinal absorption, into bone fluid. Here Ca is temporarily stored in combination with phosphate for return to the extracellular fluid (blood) during intervals between oral intakes of Ca. The net result is a conservation of Ca postprandially and a decrease in parathyroid hormone[PTH]-induced bone destruction during subsequent fasting periods. Evidence for this postulate is provided in the following 6 sequential steps from the time a Ca-containing meal is consumed until that portion of Ca stored in bone fluid is utilized during fasting periods to aid in plasma Ca maintenance. CT secretion is stimulated by feeding and subsequent digestive processes. Postprandial secretion of CT restricts the efflux of Ca from bone fluid to blood, thereby maintaining PTH secretion. In thyroid-intact [human] individuals, both PTH and CT are secreted postprandially and act in concert on Ca homeostasis. CT actively moves phosphate into bone and prevents its loss from bone fluid to blood. Postprandial storage of Ca with phosphate occurs in bone fluid of thyroid-intact individuals. This labile storage form of Ca 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 Ca for plasma Ca control. However, augmentation of osteopenic conditions could be expected if long-term low Ca intake were accompanied by a malfunction of this CT-induced system for Ca storage.