Cholecalciferol Calcifediol Calcitriol

Vitamin D3 25-Hydroxyvitamin D3 1,25-Dihydroxyvitamin D3

(25-Hydroxycholecalciferol, (1,25-Dihydroxycholecalciferol,

25(OH)D3 or calcidiol) 1,25(OH)2D3)

Figure 28.8 • Cholecalciferol bioactivation.

One of the most well-known effects of calcitriol is to maintain calcium homeostasis. Phosphate metabolism is also affected. The mechanism of action promoting Ca2+ transport in the intestine involves calcitriol-mediated formation of a calcium-binding protein, calbindin, which is known to exist in at least two forms in humans, calbindin 1, 28kDa (CALB1) and S100 calcium binding protein G (S100G), also known as calbindin-D9k. A calcium-dependent ATPase, Na+, and calbindin are necessary for intestinal Ca2+ transport and act to enhance the transcellu-lar movement resulting in increased absorption of dietary Ca2+. Transient receptor potential cation channel, subfamily V, member 6 (TRPV6), which controls the rate of cellular entry of Ca2+, is also found to be increased in intestinal cells under the control of calcitriol. Calcitriol also promotes intestinal phosphate absorption, mobilization of Ca2+ and phosphate from bone, and renal reabsorption of Ca2+ and phosphate. Also involved are parathyroid hormone and calcitonin.

VDRs have also been identified in tissues not normally associated with bone mineral homeostasis. Besides the intestines, kidneys, and osteoblasts, vitamin D receptors have been located in the parathyroid gland, the pancreatic islet cells, the mammary epithelium, the skin keratinocytes, muscle, and the immune cells. Activation in the latter has potent antiproliferative and immunomodulatory functions. Thus, calcitriol and its analogous VDR ligands have therapeutic potential in the treatment of inflammatory diseases (rheumatoid and psoriatic arthritis), dermatological conditions (psoriasis, keratosis), osteoporosis, suppression of parathyroid hormone, cancers (including colon, prostate, and breast), and autoimmune diseases.70 It has been suggested that vitamin D exerts its anticancer effects through its role as a nuclear transcription factor that regulates cell growth, dif ferentiation, apoptosis, and other cancer-developing cellular mechanisms.71

The classic form of vitamin D deficiency universally recognized is rickets. In young infants, the entire skull is soft (craniotabes), and problems in bone development lead to delays in sitting, crawling, and walking. Osteomalacia (evident on x-rays) and deformities of the bones eventually lead to deformities in the rib cage, bowlegs or knock-knees, bone pain, and a predisposition to fractures. Bone deformities may become permanent if not treated with vitamin D at an early stage. Vitamin D deficiency in children and adults also leads to myopathies, which can lead to weakness, and hypocalcemia, which can lead to paresthesia, muscle spasms, and tetany. Recent studies conclude that an increased rate of overall mortality in the general population is associated with low levels of vitamin D.72 The same study also demonstrated that vitamin D deficiency increases the risk of cancer, diabetes, and hypertension.

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