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Blood calcium levels are regulated by parathyroid hormone (PTH)    , which is produced by the parathyroid glands, as illustrated in [link] . PTH is released in response to low blood Ca 2+ levels. PTH increases Ca 2+ levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca 2+ from bone into the blood. PTH also inhibits osteoblasts, reducing Ca 2+ deposition in bone. In the intestines, PTH increases dietary Ca 2+ absorption, and in the kidneys, PTH stimulates reabsorption of the CA 2+ . While PTH acts directly on the kidneys to increase Ca 2+ reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.

The parathyroid glands, which are located in the neck, release parathyroid hormone, or PTH. PTH causes the release of calcium from bone and triggers the reabsorption of calcium from the urine in the kidneys. PTH also triggers the formation of calcitriol from vitamin D. Calcitriol causes the intestines to absorb more calcium. The result is increased calcium in the blood.
Parathyroid hormone (PTH) is released in response to low blood calcium levels. It increases blood calcium levels by targeting the skeleton, the kidneys, and the intestine. (credit: modification of work by Mikael Häggström)

Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).

The hormone calcitonin    , which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.

Hormonal regulation of growth

Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH) , produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Growth hormone has direct and indirect mechanisms of action. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a glucose-sparing effect    . In another direct mechanism, GH stimulates glycogen breakdown in the liver; the glycogen is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a diabetogenic effect    because it is similar to the high blood glucose levels seen in diabetes mellitus.

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