Evidence for an important physiological role for calcitonin

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. 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.

Ultrastructural and physiological evidence for calcitonin-induced postprandial calcium storage in bones of rats

“…These aggregates were distributed throughout the space separating bone lining cells from the mineralized bone surfaces. A similar dense material has been reported in tissue from calcitonin-injected postpartum rats [9], and from bone of normal fasted adult rats injected with calcitonin [5]. In the first report, the aggregates were stained with lanthanum.…”

“…This study now increases to four the different histological techniques that have identified bone fluid changes occurring only in or intensified by the presence of calcitonin. The two previously reported techniques [5,9] resulted from exogenous calcitonin administration and the two in this report were identified postprandially in TI rats and TX rats injected with calcitonin. Although the four methods all indicate that changes occurred in bone fluid, including the surfaces of bone, there were differences in the form and location of the calcitonin-stimulated material.…”

“…More complete details of the sequential postprandial steps in this proposed function of calcitonin have been reported (9). A crucial factor in establishing this postulate is the identification, either directly or indirectly, of calcium storage in bone following consumption of a calcium-containing meal, and the involvement of bone lining cells in this process.…”

Estimation of the C-cell numbers in rat thyroid glands using the optical fractionator.

“…This hormone has a transient inhibitory effect on bone resorption, causing a temporary decrease in blood calcium levels (Van Noorden et al, 1977;Young and Leblond, 1963;Stux et al, 1961). The major effect of CT appears to be protection of the skeleton from excessive calcium losses, but its physiological function is still unclear (Zaidi et al, 1788;Van Der Wiel and Talmage, 1981;Talmage et al, 1980;Taylor et al, 1977). Despite the fact that the effects of the hormone have been studied intensively for more than 30 years, no syndrome in humans can be attributed either to its overproduction or its def-icit (Body, 1993;Tzanela et al, 1993;Tiegs et al, 1986).…”

Calcitonin: From the Determination of Circulating Levels in Various Physiological and Pathological Conditions to the Demonstration of Lymphocyte Receptors

“…On the other hand, it was assumed that CT had an important role in the proper utilization of dietary calcium [4], However, most data had been ob tained with poorly sensitive and specific radioimmunoas says. The lack of sensitivity precluded definition of sub normal values and thus made very difficult the study of possible CT-deficiency conditions.…”