The secretion of both calcitonin and parathyroid hormone is determined by the level of calcium in the blood. When levels of calcium in the blood increase, calcitonin is secreted in higher quantities. When levels of calcium in the blood decrease, this causes the amount of calcitonin secreted to decrease too.
The secretion of calcitonin is also inhibited by the hormone somatostatin , which can also be released by the C-cells in the thyroid gland. There does not seem to be any direct deleterious effect on the body as a result of having too much calcitonin.
Medullary thyroid cancer is a rare type of cancer that arises from the C-cells in the thyroid gland that secrete calcitonin. It is sometimes associated with multiple endocrine neoplasia type 2a and multiple endocrine neoplasia type 2b.
Patients with medullary thyroid cancer have high calcitonin levels in their bloodstream. However, it is important to note that these high calcitonin levels are a consequence of this condition, not a direct causal factor. There does not seem to be any clinical effect on the body as a result of having too little calcitonin.
Patients who have had their thyroid gland removed, and have undetectable levels of calcitonin in their blood, show no adverse symptoms or signs as a result of this. About Contact Events News. Search Search. Abstract We propose that calcitonin, secreted in response to the intake of food, aids in routing calcium, obtained by intestinal absorption, into bone fluid. Publication types Research Support, U. Gov't, Non-P. Hyperplasia of C-cells occurs in response to longterm hypercalcemia.
When blood calcium is lowered, the stimulus for calcitonin secretion is diminished. Calcitonin exerts its effects by interacting with target cells, primarily in bone and kidney. The actions of PTH and calcitonin are antagonistic on bone resorption but synergistic on decreasing the renal tubular reabsorption of phosphorus. The hypocalcemic effects of calcitonin are primarily the result of decreased entry of calcium from the skeleton into plasma, resulting from a temporary inhibition of PTH-stimulated bone resorption.
The hypophosphatemia develops from a direct action of calcitonin, which increases the rate of movement of phosphorus out of plasma into soft tissue and bone and inhibits the bone resorption stimulated by PTH and other factors. Although many effects have been attributed to calcitonin at pharmacologic doses, their physiologic relevance is suspect. Physiologically, calcitonin has at best a minor role in regulating blood concentrations of calcium. Neither chronically high eg, as in animals with medullary thyroid cancer nor chronically low eg, as in animals after surgical removal of the thyroid gland circulating calcitonin concentrations result in any changes in the serum calcium concentration.
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