Abstract

An oral load of calcium with a radiocalcium trace dose was administered to totally thyroidectomized and control subjects in order to evaluate the role of the thyroid gland in the control of postprandial hypercalcemia. The following results were obtained: (1) During calcium absorption thyroidectomized subjects showed blood calcium increments significantly higher than controls. (2) Plasma radioactivity appearance curves in both thyroidectomized and control subjects were similar. (3) Any difference in the intestinal absorption of calcium was not found between the experimental groups. From the results, a difference in intestinal calcium absorption and/or in the size and turnover rate of the dilutional compartment of calcium can be ruled out as possible causes of higher blood calcium increments in thyroidectomized subjects. Therefore, impaired homeostatic control caused by the lack of calcitonin appeared to be the most satisfactory explanation for these findings. However, considering that there is only a slight difeerence in calcium increments and that calcium elevations were constantly observed also in controls, the effect of the hormone on blood calcium homeostasis appears to be of limited importance. The bone calcium-sparing effect of the hormone during post-prandial hypercalcemia in the adult can probably be considered physiologically more significant than protection against hypercalcemia.

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