Abstract

The inhibitory effect of calcitonin on bone resorption is a well documented phenomenon (5, 7). However, its physiologic importance in man is still uncertain. From earlier studies (4, 6, 9, 11) counteraction against hypercalcemia through inhibition of bone calcium resorption appeared to be the most probable role. Since physiologic hypercalcemia may be provoked by intestinal absorption of dietary calcium, the role of calcitonin has been evaluated by administering oral calcium loads to athyroid animals (3, 8). Studies in man have also been carried out (2). In the present investigation on athyroid and control subjects, a larger oral calcium load than in the previous study was administered in order to further evaluate the role of endogenous calcitonin in the control of postprandial hypercalcemia. In addition the possibility that other factors beside calcitonin are playing a role in antagonizing hypercalcemia was taken into consideration and ruled out after comparison of the curves of blood stable calcium increment and of the cumulative fractional intestinal calcium absorption.

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