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Calcitonin

Calcitonin is a 32 amino acid polypeptide hormone that is produced in humans primarily by the C cells of the thyroid, and in many other animals in the ultimobranchial body. more...

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Synthesis

It is formed by proteolytic cleavage of a larger prepropeptide which is the product of the CALC1 gene, which itself is part of a superfamily of related protein hormone precusors including Islet Amyloid Precursor Protein, Calcitonin Gene-Related Peptide and the precursor of Adrenomedullin.

Physiology

The hormone participates in calcium and phosphorus metabolism and it was found in fish, reptiles, birds and mammals. Most evidence points to that Calcitonin is not of physiological importance to humans, except for it's pharmacological use (see below).

Specifically, calcitonin reduces blood calcium levels in three ways:

  • Decreasing calcium absorption by the intestines
  • Decreasing osteoclast activity in bones
  • Decreasing calcium and phosphate reabsorption by the kidney tubules

Its actions, broadly, are:

  • Bone mineral metabolism
    • Prevent postprandial hypercalcemia resulting from absorption of Ca++ from foods during a meal
    • Promote mineralization of skeletal bone
    • Protect against Ca++ loss from skeleton during periods of Ca++ stress such as pregnancy and lactation
  • Vitamin D regulation
  • A satiety hormone
    • Inhibit food intake in rats and monkeys
    • May have CNS action involving the regulation of feeding and appetite

Like the PTH receptor, the receptor of calcitonin is a serpentine G protein-coupled receptor with seven membrane spanning regions which is coupled by Gs to adenylyl cyclase and thereby to the generation of cAMP in target cells. Indeed, the PTH and calcitonin receptors are family members which are related in amino acid sequence, though their ligands are not.

Pharmacology

Salmon calcitonin is used for the treatment of:

  • Postmenopausal osteoporosis
  • Hypercalcaemia
  • Paget's disease
  • Bone metastases

History

Calcitonin was purified in 1962 by Copp and Cheney. While it was initially considered a secretion of the parathyroid glands, it was later identified as the secretion of the C-cells (parafollicular cells) of the thyroid.

Read more at Wikipedia.org


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Daily Oral Alendronate Increases BMD Better Than Intranasal Calcitonin
From OB/GYN News, 8/1/01 by Mary Ann Moon

WASHINGTON -- Daily oral alendronate is more effective than daily intranasal calcitonin among postmenopausal women with osteoporosis, Dr. Clifford J. Rosen said at an international symposium on women's health and menopause.

Alendronate (Fosamax), a bisphosphonate that inhibits bone resorption, has been shown to increase bone mineral density and reduce fractures in osteoporosis patients. Calcitonin, a polypeptide, is thought to augment bone formation by increasing osteoblast activity, he said.

The two agents were directly compared in a 2-year, multi-center study involving 275 women with osteoporosis. "No prior study has compared therapeutic doses of alendronate and calcitonin in a parallel design," said Dr. Rosen, director of the Maine Center for Osteoporosis Research and Education at St. Joseph Hospital in Bangor.

This study was supported in part by Merck & Co. Inc., West Point, Pa., maker of Fosamax.

The study subjects were women aged 45 years and older who had been postmenopausal for at least 5 years and younger women who had undergone surgical menopause at least 5 years previously.

During the first year of the study, the subjects were randomly assigned to receive either 10 mg of oral alendronate, 200 IU of calcitonin nasal spray, or an oral placebo every day. During the second year, women who had received the placebo were switched to oral alendronate.

All patients received daily calcium and vitamin D supplements as well, Dr. Rosen said in a poster presentation at the meeting, which was also sponsored by the National Institutes of Health, the International Menopause Society, and the North American Menopause Society.

Dual x-ray absorptiometry scanning showed that alendronate produced significantly greater increases in bone mineral density at the hip trochanter, lumbar spine, and femoral neck than did calcitonin or placebo. Calcitonin outperformed placebo only at the lumbar spine site.

Alendronate also produced greater decreases in urinary Ntelopeptide and serum bone-specific alkaline phosphatase, both markers of bone turnover. Calcitonin also decreased bone-specific alkaline phosphatase levels, compared with placebo, but to a lesser degree than did alendronate.

During the second year of the study, women who switched from placebo to alendronate showed a significant increase in bone mineral density and a decrease in both biochemical markers of bone turnover, Dr. Rosen noted.

COPYRIGHT 2001 International Medical News Group
COPYRIGHT 2001 Gale Group

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