Calcitonin

Calcitonin

Calcitonin (CT) or thyrocalcitonin is secreted in the mammalian thyroid gland by parafollicular or ‘C’ cells of thyroid gland which are found in the interstitial tissue between the follicles. In reptiles, amphibians and birds, CT is secreted from ultimobranchial glands.

Calcitonin is a polypeptide hormone composed of 32 amino acid residues arranged in a straight chain with a1-7-disulphide linkage. The structure of calcitonin differs considerably between species.

Regulation of Calcitonin Secretion

Hypercalcemia and to a lesser extent increased levels of blood magnesium will stimulate CT secretion.

Glucagon, the gastro-intestinal hormones, gastrin, secretin and CCK produced by the presence of food in the GI tract are the stimulants for CT release. Glucagon with gastrin provides the most potent stimulation in the secretion of CT.

Gastro-intestinal hormones may be important in triggering the early release of calcitonin to prevent the develop­ment of hypercalcemia following the ingestion of high calcium meal.

CT protects the skeleton during Ca stress like during growth, pregnancy and lactation.

Calcitonin secretion is increased in response to a high calcium meal; often before a significant rise in plasma calcium can be detected.

Biological effects of calcitonin

With respect to plasma Calcium level, CT antagonises the actions of PTH by inhibiting osteoclastic bone resorption. Calcitonin stimulates the development of various degrees of hypocalcemia and hypophosphatemia.

Increased blood calcium level is the principle stimulus of CT release. It causes decreased movement of calcium ions from the bone calcium pool (behind the osteoblast‑osteocyte barrier) to extra cellular fluid.

Osteoclasts have receptors for calcitonin. CT decreases bone resorption through an inhibitory effect on osteo­clasts. CT also increases movement of phosphate from the extra cellular fluid into bone, thus helps deposition of Ca2+ ions by activating osteoblastic activity .

CT increases Ca2+ excretion through kidneys. It increases osteoblastic activity, but inhibits the formation of new osteoclasts from osteoprogenitor cells. The CT prevents the postprandial hypercalcemia.

CT has similar effect as PTH on renal phosphate elimination; i.e., increases phosphate elimination through kidneys by reducing phosphate resorption.

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