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

Abstract

Summary.The postulate tested by these experiments is that calcitonin directs a portion of the calcium absorbed from food into temporary storage at surfaces of bone. This study utilized young adult rats in which the parathyroid glands had been autotransplanted. Many rats were also thyroidectomized (TX). All were trained to a 0900 h feeding schedule with predetermined calcium content of food. Calcitonin was injected only during the first 4 h postprandially to some of the TX animals. Urine calcium was monitored and, after sacrifice, changes in the tibia were recorded. The following results were obtained: (a) In thyroid-intact (TI) rats, renal calcium excretion was reduced if the daily intake of calcium was less than 90 mg. In TX rats calcium excretion rose each day during the time of intestinal absorption of calcium. Calcitonin injection to TX rats reduced urinary calcium content on the day it was injected. However, on the following 2 days, renal calcium excretion rose to twice that of TX controls. (b) Electron micrographs of bone tissue from TI rats and TX rats injected with calcitonin showed greater pyroantimonate reaction within bone fluid than did tissue from TX controls. Similarly, when prepared by an anhydrous procedure, bone surfaces of tibia taken from rats with endogenous or exogenous calcitonin contained dense material accumulation (following a calcium-containing meal) not present in bones from TX rats. (c) When tibia shaft fragments of rats sacrificed 4 h after consuming a calcium-containing meal were washed in acidic saline, more calcium accumulated during the first 15 min in the media containing bones from TI than from TX rats. The final equilibration level between media and bone fragments was not affected by the calcitonin state of the rat. These experiments demonstrate both physiological and bone morphological differences between TI and TX rats which Send offprint requests to C. J. VanderWiel at the above address.can be negated by postprandial calcitonin injection to TX animals. They support the postulate that the secretion of calcitonin postprandially aids in the conservation and storage of ingested calcium.Key words: Calcitonin --Calcium conservation --Calcium storage --Bone ultrastructure.A definitive role for calcitonin in the normal physiology of man and other mammals has not yet been established. Even though the presence of calcitonin has been identified in plasma of all mammals studied, there is as yet no evidence that its deficiency or absence causes a detectable health problem.It has been proposed that calcitonin may be a digestion-related hormone functioning to conserve and store dietary calcium [1][2][3]. In an extension of these ideas, we have postulated that postprandial calcitonin secretion directs calcium obtained during intestinal absorption into the bone fluid for temporary storage [4]. It is suggested that a portion of the dietary calcium is retained as a calcium phosphate colloid which is prevented from crystallizing into hydroxyapatite by the presence of a mineralization inhibitor....

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).…”

Reduction of lead-induced hypercalcemia by calcitonin: Comparison between thyroid-intact and thyroidectomized rats

“…In the accompanying paper [18] it is reported that the effect of calcitonin on lead-induced hypercalcemia and hyperphosphatemia is accompanied by unique cytological reactions within endosteal bone lining cells from tibia of rats. Lead is known to have a high affinity for phosphate and is often used as a stain for this anion [19].…”