Effects of Hypercalcemia and Hypocalcemia on the Thyrocalcitonin Content of Rat Thyroid Glands

Abstract

Systemic hypercalcemia induced in intact rats by ip injection of CaCk, gavage feeding of Ca lactate, or a very high calcium diet, consistently reduced the thyrocalcitonin (TC) content of the thyroid gland measured by biological assay. Maximal reduction to 35 ±5% of the content in normocalcemic controls was noted as early as 2 hr after the induction of hypercalcemia. Large doses of vit. D or prolongation of dietary hypercalcemia to 23 days did not decrease the content further. Recovery to a normal content was noted 16 hr after the end of a hypercalcemia of 2 hr. The chronic hypocalcemia of parathyroidectomized rats kept on normal diet was associated with a progressive accumulation of TC in the thyroid gland. A 12-fold increase in the content was present after 14 weeks, the longest interval studied. Restoration of normocalcemia with 4 parathyroid homografts or the delayed induction of chronic dietary hypercalcemia bothsignificantly reduced but did not eliminate the TC accumulation in such rats. The absence of parathyroid tissue during a hypercalcemia did not alter the amount of residual TC detectable in the thyroid, negating the role of a TC-releasing factor from the parathyroid. We conclude that in the rat systemic hypercalcemia is a stimulus for the rapid release of TC. The results suggest that TC is available to combat only brief challenges of hypercalcemia. The accumulation of TC in the thyroid of chronically hypocalcemic rats is viewed as the result of continuing synthesis in the absence of normal stimuli for release. This interpretation and a partial reversal of the accumulation of TC when such rats were made normocalcemic by parathyroid homografts both suggest an active role for TC in the maintenance of normocalcemia in rats. (Endocrinology82: 83, 1968)