Dihydroxycholecalciferol: Difference between revisions

Latest revision as of 12:40, 31 December 2024

Dihydroxycholecalciferol[edit]

Dihydroxycholecalciferol, also known as calcitriol, is the active form of vitamin D in the human body. It plays a crucial role in maintaining calcium and phosphate homeostasis, which is essential for healthy bone formation and maintenance.

Biochemistry[edit]

Dihydroxycholecalciferol is synthesized in the body from cholecalciferol (vitamin D3) through a series of hydroxylation reactions. The first hydroxylation occurs in the liver, converting cholecalciferol to 25-hydroxycholecalciferol (calcidiol). The second hydroxylation takes place in the kidneys, where calcidiol is converted to calcitriol.

Physiological Role[edit]

Calcitriol functions as a hormone that regulates the levels of calcium and phosphate in the bloodstream. It enhances the absorption of calcium and phosphate from the intestine, promotes the reabsorption of calcium in the kidneys, and mobilizes calcium from the bones when necessary.

Calcium Homeostasis[edit]

Calcitriol increases the expression of calcium-binding proteins in the intestinal epithelium, facilitating the efficient absorption of dietary calcium. It also acts on the renal tubules to reduce the excretion of calcium, thus conserving it in the body.

Bone Health[edit]

By maintaining adequate levels of calcium and phosphate, calcitriol ensures proper mineralization of the bone matrix. It works in concert with parathyroid hormone (PTH) to regulate bone remodeling and turnover.

Clinical Significance[edit]

Deficiency[edit]

A deficiency in calcitriol can lead to rickets in children and osteomalacia in adults, conditions characterized by softening and weakening of the bones. This deficiency is often due to inadequate dietary intake of vitamin D, insufficient sunlight exposure, or disorders affecting the liver or kidneys.

Excess[edit]

Excessive levels of calcitriol can result in hypercalcemia, a condition marked by elevated calcium levels in the blood. Symptoms of hypercalcemia include nausea, vomiting, weakness, and in severe cases, cardiac arrhythmias and kidney stones.

Therapeutic Use[edit]

Calcitriol is used therapeutically to treat conditions such as hypocalcemia in patients with chronic kidney disease, hypoparathyroidism, and certain types of psoriasis. It is available in oral and intravenous formulations.

Synthesis and Metabolism[edit]

The synthesis of calcitriol is tightly regulated by the body. Factors such as parathyroid hormone levels, serum calcium, and phosphate concentrations influence the activity of the enzyme 1-alpha-hydroxylase in the kidneys, which is responsible for the final step in calcitriol synthesis.

@@ Line 1: / Line 1: @@
-Dihydroxycholecalciferol, also known as calcitriol, is a biologically active form of vitamin D. It plays a crucial role in regulating calcium and phosphate levels in the body, as well as promoting bone health and supporting various physiological processes. This article will provide an overview of dihydroxycholecalciferol, its functions, sources, and related health implications.
+==Dihydroxycholecalciferol==
-== Overview ==
+'''Dihydroxycholecalciferol''', also known as '''calcitriol''', is the active form of vitamin D in the human body. It plays a crucial role in maintaining calcium and phosphate homeostasis, which is essential for healthy bone formation and maintenance.
-Dihydroxycholecalciferol is a hormone-like substance that is synthesized in the body from its precursor, cholecalciferol (vitamin D3). It is the most active form of vitamin D and is primarily produced in the kidneys. Dihydroxycholecalciferol acts as a hormone by binding to vitamin D receptors (VDRs) in various target tissues, including the intestines, bones, and kidneys.
-== Functions ==
+==Biochemistry==
-The primary function of dihydroxycholecalciferol is to regulate calcium and phosphate homeostasis in the body. It enhances the absorption of calcium and phosphate from the intestines, promotes their reabsorption in the kidneys, and stimulates the release of calcium from bones when needed. This hormone also plays a role in cell growth, immune function, and the modulation of gene expression.
+Dihydroxycholecalciferol is synthesized in the body from [[cholecalciferol]] (vitamin D3) through a series of hydroxylation reactions. The first hydroxylation occurs in the liver, converting cholecalciferol to [[25-hydroxycholecalciferol]] (calcidiol). The second hydroxylation takes place in the kidneys, where calcidiol is converted to calcitriol.
-== Sources ==
+==Physiological Role==
-Dihydroxycholecalciferol can be obtained through various sources. The most significant source is sunlight exposure, as the skin can synthesize cholecalciferol when exposed to ultraviolet B (UVB) radiation. Additionally, certain foods such as fatty fish (e.g., salmon, mackerel), egg yolks, and fortified dairy products contain small amounts of vitamin D3. Dietary supplements are also available for individuals who have limited sun exposure or inadequate dietary intake.
+Calcitriol functions as a hormone that regulates the levels of calcium and phosphate in the bloodstream. It enhances the absorption of calcium and phosphate from the [[intestine]], promotes the reabsorption of calcium in the [[kidneys]], and mobilizes calcium from the [[bone]]s when necessary.
-== Health Implications ==
+===Calcium Homeostasis===
-A deficiency of dihydroxycholecalciferol can lead to various health problems. Insufficient levels of this hormone can result in impaired calcium absorption, leading to weakened bones and an increased risk of fractures. In children, vitamin D deficiency can cause rickets, a condition characterized by soft and weak bones. In adults, it can contribute to osteoporosis, a condition characterized by reduced bone density and increased fracture risk.
+Calcitriol increases the expression of calcium-binding proteins in the intestinal epithelium, facilitating the efficient absorption of dietary calcium. It also acts on the renal tubules to reduce the excretion of calcium, thus conserving it in the body.
-On the other hand, excessive levels of dihydroxycholecalciferol can also have adverse effects. Hypercalcemia, a condition characterized by high levels of calcium in the blood, can occur due to excessive vitamin D intake. This can lead to symptoms such as nausea, vomiting, constipation, and even kidney damage.
+===Bone Health===
+By maintaining adequate levels of calcium and phosphate, calcitriol ensures proper mineralization of the bone matrix. It works in concert with [[parathyroid hormone]] (PTH) to regulate bone remodeling and turnover.
-== See Also ==
+==Clinical Significance==
+===Deficiency===
+A deficiency in calcitriol can lead to [[rickets]] in children and [[osteomalacia]] in adults, conditions characterized by softening and weakening of the bones. This deficiency is often due to inadequate dietary intake of vitamin D, insufficient sunlight exposure, or disorders affecting the liver or kidneys.
+===Excess===
+Excessive levels of calcitriol can result in [[hypercalcemia]], a condition marked by elevated calcium levels in the blood. Symptoms of hypercalcemia include nausea, vomiting, weakness, and in severe cases, cardiac arrhythmias and kidney stones.
+==Therapeutic Use==
+Calcitriol is used therapeutically to treat conditions such as [[hypocalcemia]] in patients with chronic kidney disease, [[hypoparathyroidism]], and certain types of [[psoriasis]]. It is available in oral and intravenous formulations.
+==Synthesis and Metabolism==
+The synthesis of calcitriol is tightly regulated by the body. Factors such as [[parathyroid hormone]] levels, serum calcium, and phosphate concentrations influence the activity of the enzyme 1-alpha-hydroxylase in the kidneys, which is responsible for the final step in calcitriol synthesis.
+==See Also==
 * [[Vitamin D]]
-* [[Cholecalciferol]]
+* [[Calcium metabolism]]
-* [[Calcium]]
+* [[Bone mineral density]]
-* [[Osteoporosis]]
-== References ==
+{{Vitamin D}}
-<references>
+{{Hormones}}
-<ref>Smith A, Jones B. Role of dihydroxycholecalciferol in calcium homeostasis. J Endocrinol. 2020;246(1):R1-R10.</ref>
-<ref>Wang Y, Zhu J, DeLuca HF. Where is the vitamin D receptor? Arch Biochem Biophys. 2012;523(1):123-133.</ref>
-<ref>Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281.</ref>
-</references>
 [[Category:Vitamins]]