By Sally Robertson, BSc
Calcitonin is a protein hormone that, in humans and other mammals, is mainly secreted by the parafollicular cells (C cells) of the thyroid gland. This hormone is also referred to as thyrocalcitonin. In humans, calcitonin is made up of 32 amino acids. In nonmamallian animals such as fish and birds, calcitonin is secreted by cells in the glandular ultimobranchial bodies.
Its main actions are to increase bone calcium content and decrease the blood calcium level when it rises above normal. It also lowers the blood phosphorus level when that rises above normal. Calcitonin opposes the effects of parathyroid hormone, which acts to increase the blood level of calcium. Parathyroid hormone achieves this through several actions involving the bones, kidneys and intestine. It stimulates the release of calcium from the bones where it is stored in large amounts, thereby increasing bone destruction and decreasing new bone formation. It lowers the amount of calcium lost in the urine and stimulates active vitamin D production in the kidneys. It also increases the amount of calcium absorbed from food in the intestine via its effects on vitamin D metabolism.
Some examples of calcitonin’s actions are described below:
- Calcitonin prevents calcium loss from bones, which is particularly important in conditions that tend to lead to calcium loss such as pregnancy or being immobilized for a prolonged period due to a fracture or heart attack. Calcium being lost from the bones can make them brittle, fragile and prone to fracture.
- Calcitonin helps maintain a normal level of blood calcium, mainly by preventing the calcium level from rising above normal after a meal. One way calcitonin does this is by preventing the absorption of calcium from the intestine.
- Calcitonin plays a role in maintaining normal blood levels of Vitamin D.
- Calcitonin suppresses the activity of cells in the bone called osteoclasts. Osteoclasts dissolve bone tissue, which is replaced by new tissue formed by cells called osteoblasts. Calcitonin acts on receptors present on the surface of osteoclasts to stop them from breaking down bone. Under the microscope, the binding of calcitonin to its receptor appears to cause the osteoclasts to lose their “ruffled border,” which refers to the compactly folded cell membrane that aids bone removal by increasing the cell’s surface area for resorption.
- Calcitonin also regulates the level of calcium and other mineral levels in the kidneys. It prevents the re-absorption of phosphate by the kidney and increases the kidney’s re-absorption of calcium and magnesium, leading to increased calcium excretion via the urine.
- In some mammals, calcitonin seems to play a role in hunger and satiety.
- The rate of bone loss is accelerated in post-menopausal women and in those with osteoporosis, where thinning of the bone arises due to decreased bone formation or increased bone resorption, calcitonin has been shown to improve the density and strength of bone.
- Examples of conditions that are treated using calcitonin include Paget’s disease of the bone and hypercalcemia (chronically high blood calcium). Paget’s disease leads to an accelerated and disorderly remodelling of the bone which causes the bones to become painful and weak. Calcitonin reduces bone turnover in these patients and in 1991, an intranasal calcitonin spray was approved by The Food and Drug Administration for treatment of the condition.
Both increased calcitonin secretion and activity only last a few days and patients with hypercalcemia do not have a high serum level of calcitonin. In patients with medullary thyroid carcinoma, on the other hand, cancerous C cells secrete large amounts of calcitonin. These patients have a high level of serum calcitonin but a normal level of serum calcium. Other conditions where the calcitonin concentration may also be increased include lung cancer and some pancreatic tumors, specifically, a tumor that secretes insulin referred to as insulinoma and a vasoactive intestinal polypeptide-secreting tumor referred to as VIPoma.
Last Updated: Jul 22, 2015