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Calcitriol ( INN ), also called 1,25-dihydroxycholecalciferol, or 1alpha,25-dihydroxyvitamin D3, 1,25-dihydroxyvitamin D 3 and other variants, is the hormonally active metabolite of vitamin D which has three hydroxyl groups. It can be abbreviated 1α,25-(OH) 2 D 3 or simply 1,25(OH) 2 D.
1 Nomenclature
2 Function
3 Biosynthesis and its regulation
4 Metabolism
5 Medical use
6 Adverse effects
7 History
8 Interactive pathway map
9 Additional images
10 See also
11 References
Calcitriol usually refers specifically to 1,25-dihydroxycholecalciferol. Because cholecalciferol already has one hydroxyl group, only two (1,25) are further specified in this nomenclature, but there are three (1,3,25-triol), as indicated in when calcitriol is used. The 1-hydroxy group is in the alpha position, and this may be specified in the name, for instance in the abbreviation 1α,25-(OH) 2 D 3.
Calcitriol is the strictly the 1-hydroxylation product of calcifediol (25-OH vitamin D 3 ), derived from cholecalciferol (vitamin D 3 ), rather than the product of hydroxylations of ergocalciferol (vitamin D 2 ).
Calcitriol is marketed as a pharmaceutical for medical use under various trade names including Rocaltrol ( Roche ), Calcijex ( Abbott ), Decostriol (Mibe, Jesalis), Vectical ( Galderma ), and Rolsical ( Sun Pharma ).
Calcitriol increases blood calcium levels ([ Ca 2+ ]) by:
Promoting absorption of dietary calcium from the gastrointestinal tract.
Increasing renal tubular reabsorption of calcium, thus reducing the loss of calcium in the urine.
Stimulating release of calcium from bone. For this it acts on the specific type of bone cells referred to as osteoblasts, causing them to release RANKL, which in turn activates osteoclasts.
Calcitriol acts in concert with parathyroid hormone (PTH) in all three of these roles. For instance, PTH also indirectly stimulates osteoclasts. However, the main effect of PTH is to increase the rate at which the kidneys excrete inorganic phosphate (P i ), the counterion of Ca 2+. The resulting decrease in serum phosphate causes hydroxyapatite (Ca 5 (PO 4 ) 3 OH) to dissolve out of bone thus increasing serum calcium. PTH also stimulates the production of calcitriol (see below).
Many of the effects of calcitriol are mediated by its interaction with the calcitriol receptor, also called the vitamin D receptor or VDR. For instance, the unbound inactive form of the calcitriol receptor in intestinal epithelial cells resides in the cytoplasm. When calcitriol binds to the receptor, the ligand -receptor complex translocates to the cell nucleus, where it acts as a transcription factor promoting the expression of a gene encoding a calcium binding protein. The levels of the calcium binding protein increase enabling the cells to actively transport more calcium ( Ca 2+ ) from the intestine across the intestinal mucosa into the blood.
The maintenance of electroneutrality requires that the transport of Ca 2+ ions catalyzed by the intestinal epithelial cells be accompanied by counterions, primarily inorganic phosphate. Thus calcitriol also stimulates the intestinal absorption of phosphate.
The observation that calcitriol stimulates the release of calcium from bone seems contradictory, given that sufficient levels of serum calcitriol generally prevent overall loss of calcium from bone. It is believed that the increased levels of serum calcium resulting from calcitriol-stimulated intestinal uptake causes bone to take up more calcium than it loses by hormonal stimulation of osteoclasts. Only when there are conditions, such as dietary calcium deficiency or defects in intestinal transport, which result in a reduction of serum calcium does an overall loss of calcium from bone occur.
Calcitriol also inhibits the release of calcitonin,
Biosynthesis and its regulation
Calcitriol is produced in the cells of the proximal tubule of the nephron in the kidneys by the action of 25-hydroxyvitamin D 3 1-alpha-hydroxylase, a mitochondrial oxygenase and an enzyme which catalyzes the hydroxylation of 25-hydroxycholecalciferol (calcifediol) in the 1-alpha position.
The activity of this enzyme is stimulated by PTH. This is an important control point in Ca 2+ homeostasis.
Calcitriol is also produced outside the kidney in small amounts by many other tissues including placenta and activated macrophages.
When the drug alfacalcidol is used, 25-hydroxylation in the liver will produce calcitriol as the active metabolite. This will produce greater effects than other vitamin D precursors in patients with kidney disease who have loss of the renal 1-alpha-hydroxylase.
Calcitriol’s lifespan in the body is measured in hours, unlike its precursor calcifediol whose lifespan is measured in weeks. Calcitroic acid is more soluble in water and is excreted in bile and urine.
Medical use
Calcitriol is prescribed for:
Treatment of hypocalcaemia – hypoparathyroidism, osteomalacia (adults), rickets (infants, children), renal osteodystrophy, chronic kidney disease
Treatment of osteoporosis
Prevention of corticosteroid-induced osteoporosis
Calcitriol has been used in an ointment for the treatment of psoriasis,
Adverse effects
The main adverse drug reaction associated with calcitriol therapy is hypercalcemia – early symptoms include: nausea, vomiting, constipation, anorexia, apathy, headache, thirst, pruritus, sweating, and/or polyuria. Compared to other vitamin D compounds in clinical use ( cholecalciferol, ergocalciferol ), calcitriol has a higher risk of inducing hypercalcemia. However, such episodes may be shorter and easier to treat due to its relatively short half-life.
It was first identified in 1971 by Michael F. Holick working in the laboratory of Hector DeLuca,
Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles.
|{{{bSize}}}px|alt=Vitamin D Synthesis Pathway ( view / edit )]]
Vitamin D Synthesis Pathway ( view / edit )
^ The interactive pathway map can be edited at WikiPathways: “VitaminDSynthesis_WP1531”.
Additional images
Calcitriol synthesis
See also
Vitamin D
Calcium metabolism
Calcitroic acid

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