Clinical physiology

Vitamin D and its active metabolites, parathyroid hormone (PTH) and calcitonin, are the principal regulators of calcium metabolism. When plasma calcium falls, PTH release leads immediately to decreased renal calcium excretion and, in conjunction with 1,25-dihydroxyvitamin D, mobilization of calcium from bone. A slower action is to promote calcium and phosphate absorption from the gut. An undesirable rise in plasma phosphate concentration is prevented by the phosphaturic effect of PTH. Hypercalcemia inhibits PTH which leads to increased calcium excretion, decreased bone resorption and suppression of calcium binding in the gut. Serum phosphate concentrations are less strictly controlled; phosphate loss increases Vitamin D synthesis independently of PTH and phosphate retention inhibits it.

Vitamin D3, cholecalciferol, is produced in the skin as a result of exposure of 7-dehydrocholesterol to ultraviolet light via a previtamin D3 which undergoes slow conversion to cholecalciferol at body temperature. This has a high affinity for the Vitamin D binding protein, an α2-globulin synthesized in the liver, whereas the previtamin remains in the skin. An excess of sunlight converts previtamin D3 to inactive compounds thus preventing Vitamin D intoxication after sunbathing. Vitamin D may also be ingested and absorbed with chylomicrons. The concentration of the Vitamin D binding protein far exceeds the requirement for Vitamin D transport and it thereby acts as a reservoir supplying free Vitamin D metabolites to the cells.