Calcitriol

Calcitriol is the active form of vitamin D, normally made in the kidney.

Instead it could be considered a hormone, with activation of the vitamin D pro-hormone resulting in the active form, calcitriol, which then produces effects via a nuclear receptor in multiple locations.

Calcitriol is the active form of vitamin D, normally made in the kidney.

For example, they convert a precursor of vitamin D to its active form, calcitriol; and synthesize the hormones erythropoietin and renin.

Calcitriol increases blood calcium (Ca 2+ ) mainly by increasing the uptake of calcium from the intestines.

Parathyroid hormone secreted by the parathyroid gland regulates the resorption of Ca 2+ from bone, reabsorption in the kidney back into circulation, and increases in the activation of vitamin D 3 to calcitriol.

A manufactured form is used to treat kidney disease with low blood calcium, hyperparathyroidism due to kidney disease, low blood calcium due to hypoparathyroidism, osteoporosis, osteomalacia, and familial hypophosphatemia.

Calcitriol has been used in an ointment for the treatment of psoriasis, although the vitamin D analogue calcipotriol (calcipotriene) is more commonly used.

Calcipotriol, also known as calcipotriene, is a synthetic derivative of calcitriol, a form of vitamin D.

A manufactured form is used to treat kidney disease with low blood calcium, hyperparathyroidism due to kidney disease, low blood calcium due to hypoparathyroidism, osteoporosis, osteomalacia, and familial hypophosphatemia.

It is also treated with medications including human growth hormone, calcitriol, and phosphate.

A manufactured form is used to treat kidney disease with low blood calcium, hyperparathyroidism due to kidney disease, low blood calcium due to hypoparathyroidism, osteoporosis, osteomalacia, and familial hypophosphatemia.

A manufactured form is used to treat kidney disease with low blood calcium, hyperparathyroidism due to kidney disease, low blood calcium due to hypoparathyroidism, osteoporosis, osteomalacia, and familial hypophosphatemia.

This typically occurs when the 1,25 dihydroxyvitamin D 3 levels in the blood are low and hypocalcemia is present.

Low activated vitamin D 3 levels are a result of the damaged kidneys' inability to convert vitamin D 3 into its active form, calcitriol, and result in further hypocalcaemia.

Many of the effects of calcitriol are mediated by its interaction with the calcitriol receptor, also called the vitamin D receptor or VDR.

Calcitriol, the active form of vitamin D, binds to the VDR, which then forms a heterodimer with the retinoid-X receptor.

Compared to other vitamin D compounds in clinical use (cholecalciferol, ergocalciferol), calcitriol has a higher risk of inducing hypercalcemia.

It is converted in the liver to calcifediol (25-hydroxyvitamin D) which is then converted in the kidney to calcitriol (1,25-dihydroxyvitamin D).

Serious side effects may include high blood calcium and anaphylaxis.

These plants contain calcitriol or similar substances that cause rises in calcium ion levels.

Calcitriol acts in concert with parathyroid hormone (PTH) in all three of these roles.

A third important effect of PTH on the kidney is its stimulation of the conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol), which is released into the circulation.

A manufactured form is used to treat kidney disease with low blood calcium, hyperparathyroidism due to kidney disease, low blood calcium due to hypoparathyroidism, osteoporosis, osteomalacia, and familial hypophosphatemia.

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.

Calcifediol is then converted in the kidneys (by the enzyme 25(OH)D-1α-hydroxylase) into calcitriol (1,25-(OH) 2 D 3 ), a secosteroid hormone that is the active form of vitamin D. It can also be converted into 24-hydroxycalcidiol in the kidneys via 24-hydroxylation.

It was first identified in 1971 by Michael F. Holick working in the laboratory of Hector DeLuca, and also by Tony Norman and colleagues.

Michael F. Holick (born 1946) is an American adult endocrinologist, specializing in the field of vitamin D, such as the identification of both calcidiol, the major circulating form of vitamin D, and calcitriol, the active form of vitamin D. His work has been the basis for diagnostic tests and therapies for vitamin D-related diseases.

This occurs through the action of the CYP24A1 24-hydroxylase.

It is a mitochondrial monooxygenase which catalyzes reactions including 24-hydroxylation of calcitriol (1,25-dihydroxyvitamin D 3 ).

Compared to other vitamin D compounds in clinical use (cholecalciferol, ergocalciferol), calcitriol has a higher risk of inducing hypercalcemia.

The binding affinity of ercalcitriol to the vitamin D receptor is similar to that of calcitriol.

Activity is also decreased by high levels of serum phosphate and by an increase in the production of the hormone FGF23 by osteocyte cells in bone.

FGF23 is secreted by osteocytes in response to elevated calcitriol.

When the drug alfacalcidol is used, 25-hydroxylation in the liver will produce calcitriol as the active metabolite.

Alfacalcidol has a weaker impact on calcium metabolism and parathyroid hormone levels than calcitriol, however alfacalcidol has significant effects on the immune system, including regulatory T cells.

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.

Expression of S100G, like that of calbindin 1, is stimulated by the active vitamin D metabolite, calcitriol although the precise mechanisms are still controversial.

Calcitriol is inactivated by further hydroxylation to form 1,24,25-trihydroxyvitamin D, calcitroic acid.

Calcitroic acid (1α-hydroxy-23-carboxy-24,25,26,27-tetranorvitamin D 3 ) is a major metabolite of 1α,25-dihydroxyvitamin D 3 (calcitriol).

This is an important control point in Ca 2+ homeostasis.

Calcium release from bone is regulated by parathyroid hormone in conjunction with calcitriol manufactured in the kidney under the influence of PTH.

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 enzyme catalyzes the hydroxylation of Calcifediol to calcitriol (the bioactive form of Vitamin D):