query: the active form of vitamin d also known as a hormone is called

pos: Vitamin D D pro-hormone resulting in the active form, calcitriol, which then produces effects via a nuclear receptor in multiple locations. Cholecalciferol is converted in the liver to calcifediol (25-hydroxycholecalciferol); ergocalciferol is converted to 25-hydroxyergocalciferol. These two vitamin D metabolites (called 25-hydroxyvitamin D or 25(OH)D) are measured in serum to determine a person's vitamin D status. Calcifediol is further hydroxylated by the kidneys to form calcitriol (also known as 1,25-dihydroxycholecalciferol), the biologically active form of vitamin D. Calcitriol circulates as a hormone in the blood, having a major role regulating the concentration of calcium and phosphate, and promoting the healthy growth and

pos: Vitamin D deficiency in Australia the body, sustaining good bone health as well as muscle function. When calcium in the body becomes under provided for normal bodily functions, calcitriol, an active form of Vitamin D, pairs with parathyroid hormone. Together they act to assemble cells in order to increase the calcium stores taken from bone. The popular term Sunshine vitamin, as it’s often called, is one of the one main sources of achieving sufficient Vitamin D through sunlight on the skin known as D3. The second form is commonly known as D2, which is found in foods such as fatty fish and fortified products like

pos: Parathyroid hormone is its stimulation of the conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates calcium uptake from the intestine. Via the kidney, PTH enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-hydroxyvitamin D 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of

pos: Endocrine bone disease women but men can be diagnosed with this silent disease as well as it mainly affects elderly individual. In addition to the thyroid gland, Vitamin D plays a crucial role in the absorption of calcium. In fact, Vitamin D is needed for efficient absorption of calcium and therefore proper bone health. Vitamin D is a fat-soluble vitamin, as well, it is unique because it is considered as a hormone; synthesized endogenously in the liver in form of Cholecalciferol. The endogenous inactive form of Vitamin D is Cholecalciferol or Vitamin D3 which is converted to active form of Vitamin D–Calcitriol also

pos: Calcifediol Calcifediol Calcifediol (INN), also known as calcidiol, 25-hydroxycholecalciferol, or 25-hydroxyvitamin D (abbreviated 25(OH)D), is a prehormone that is produced in the liver by hydroxylation of vitamin D (cholecalciferol) by the enzyme cholecalciferol 25-hydroxylase which was isolated by Michael F. Holick. Physicians worldwide measure this metabolite to determine a patient's vitamin D status. At a typical daily intake of vitamin D3, its full conversion to calcifediol takes approximately 7 days. Calcifediol is then converted in the kidneys (by the enzyme 25(OH)D-1α-hydroxylase) into calcitriol (1,25-(OH)D), a secosteroid hormone that is the active form of vitamin D. It can also be converted into

pos: Calcitriol receptor Calcitriol receptor The calcitriol receptor, more commonly known as the vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors. Calcitriol, the active form of vitamin D, binds to the VDR, which then forms a heterodimer with the retinoid-X receptor. This then binds to hormone response elements on DNA resulting in expression or transrepression of specific geneproducts. The VDR not only regulates transcriptional responses but also involved in microRNA-directed post transcriptional mechanisms. In humans, the vitamin D receptor is encoded by the

pos: Immune system system. For example, female sex hormones are known immunostimulators of both adaptive and innate immune responses. Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty. By contrast, male sex hormones such as testosterone seem to be immunosuppressive. Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D. When a T-cell encounters a foreign pathogen, it extends a vitamin D receptor. This is essentially a signaling device that allows the T-cell to bind to the active form of vitamin D, the steroid hormone calcitriol. T-cells

pos: Vitamin D In 1971–72, the further metabolism of vitamin D to active forms was discovered. In the liver, vitamin D was found to be converted to calcifediol. Calcifediol is then converted by the kidneys to calcitriol, the biologically active form of vitamin D. Calcitriol circulates as a hormone in the blood, regulating the concentration of calcium and phosphate in the bloodstream and promoting the healthy growth and remodeling of bone. The vitamin D metabolites, calcifediol and calcitriol, were identified by competing teams led by Michael F. Holick in the laboratory of Hector DeLuca and by Tony Norman and colleagues. There is considerable

pos: Calcitriol receptor the induction of these pathways during the postnatal hair cycle. These studies have revealed novel actions of the unliganded VDR in regulating the post-morphogenic hair cycle. Calcitriol receptor has been shown to interact with Calcitriol receptor The calcitriol receptor, more commonly known as the vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors. Calcitriol, the active form of vitamin D, binds to the VDR, which then forms a heterodimer with the retinoid-X receptor. This then binds to hormone response elements on

pos: Calcium in biology mineral storage site. Calcium ions, Ca, are released from bone into the bloodstream under controlled conditions. Calcium is transported through the bloodstream as dissolved ions or bound to proteins such as serum albumin. Parathyroid hormone secreted by the parathyroid gland regulates the resorption of Ca from bone, reabsorption in the kidney back into circulation, and increases in the activation of vitamin D to calcitriol. Calcitriol, the active form of vitamin D, promotes absorption of calcium from the intestines and bones. Calcitonin secreted from the parafollicular cells of the thyroid gland also affects calcium levels by opposing parathyroid hormone; however, its

pos: Hormone receptor androgens (androgen receptors), thyroid hormone (T3) (thyroid hormone receptors), calcitriol (the active form of vitamin D) (calcitriol receptors), and the retinoids (vitamin A) (retinoid receptors). Receptor-protein interactions induce the uptake and destruction of their respective hormones in order to regulate their concentration in the body. This is especially important for steroid hormones because many body systems are entirely steroid dependent. For some of these classes, in any given species (such as, for example, humans), there is a single molecule encoded by a single gene; in other cases, there are several molecules in the class. Hormone receptor A hormone receptor is

pos: Alfacalcidol hydroxylation step required for the formation of the physiologically active form of vitamin D, 1,25-dihydroxyvitamin D3. Alfacalcidol is an active vitamin D3 metabolite, and therefore does not require the second hydroxylation step in the kidney. Used as a poultry feed additive, it prevents tibial dyschondroplasia and increases phytate bioavailability. Pharmaceutical trade names include AlphaD and One-Alpha. Alfacalcidol Alfacalcidol (or 1-hydroxycholecalciferol) is an analogue of vitamin D used for supplementation in humans and as a poultry feed additive. Alfacalcidol has a weaker impact on calcium metabolism and parathyroid hormone levels than calcitriol, however alfacalcidol has significant effects on the immune system,

pos: Immune system have a symbiotic relationship with vitamin D. Not only does the T-cell extend a vitamin D receptor, in essence asking to bind to the steroid hormone version of vitamin D, calcitriol, but the T-cell expresses the gene CYP27B1, which is the gene responsible for converting the pre-hormone version of vitamin D, calcidiol into the steroid hormone version, calcitriol. Only after binding to calcitriol can T-cells perform their intended function. Other immune system cells that are known to express CYP27B1 and thus activate vitamin D calcidiol, are dendritic cells, keratinocytes and macrophages. It is conjectured that a progressive decline in hormone

pos: Calcium metabolism the plasma ionized calcium level, even though the total calcium concentration might be lowered. The kidney influences the plasma ionized calcium concentration in yet another manner. It processes vitamin D into calcitriol, the active form that is most effective in promoting the intestinal absorption of calcium. This conversion of vitamin D into calcitriol, is also promoted by high plasma parathyroid hormone levels. Most excretion of excess calcium is via the bile and feces, because the plasma calcitriol levels (which ultimately depend on the plasma calcium levels) regulate how much of the biliary calcium is reabsorbed from the intestinal contents. Urinary

pos: Senior dog diet health of dogs. In order for calcium to be properly absorbed into the body dogs will require another nutrient, vitamin D. adequate vitamin D is needed to form enough calcitriol, known as the active form of vitamin D. If enough is not present the body will begin to draw from stores of vitamin D within the body like the bones and teeth for its needs. This can lead to bone weakening and the inability to repair bone damage. Beet pulp is a common ingredient in dog diets as it is a very versatile and useful fiber source. Beet pulp provides

pos: Cholecalciferol safe medicines needed in a health system. Cholecalciferol is available as a generic medication and over the counter. Cholecalciferol is a form of vitamin D which is naturally synthesized in skin and functions as a pro-hormone, being converted to calcitriol. This is important for maintaining calcium levels and promoting bone health and development. As a medication, cholecalciferol may be taken as a dietary supplement to prevent or to treat vitamin D deficiency. One gram is 40,000,000 (40x10) IU, equivalently 1 IU is 0.025 µg. Dietary reference intake values for vitamin D (cholecalciferol and/or ergocalciferol) have been established and recommendations vary

pos: Hypocalcaemia recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth. Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH induces the kidneys to reabsorb calcium, the kidneys to increase production of calcitriol (the active form of vitamin D) thereby increasing intestinal absorption of calcium, and the bones to release calcium. These actions lead to a re-balance in the blood calcium levels. However, in the setting of absent, decreased, or ineffective PTH hormone, the body

pos: Alfacalcidol Alfacalcidol Alfacalcidol (or 1-hydroxycholecalciferol) is an analogue of vitamin D used for supplementation in humans and as a poultry feed additive. 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. It is considered to be a more useful form of vitamin D supplementation, mostly due to much longer half-life and lower kidney load. It is the most commonly prescribed vitamin D metabolite for patients with end stage renal disease, given that impaired renal function alters the ability to carry out the second

pos: Eldecalcitol osteoclast activity. Osteoblast activity serves this function of maintaining appropriate calcium levels by depositing calcium in bones when blood calcium levels are above normal. In contrast, osteoclasts break down bone tissue to increase blood calcium levels if they are low. This activity is performed after absorption of calcium by the body, which requires the actions of vitamin D. The active metabolite of vitamin D, calcitriol, performs its function through interactions with the calcitriol receptor. This nuclear hormone receptor is responsible for calcium absorption which, in turn, is involving in bone depletion and formation. The new analogs of vitamin D, such

pos: Vitamin D of the kidneys, where it is hydroxylated at the 1-α position (lower right of the molecule) to form calcitriol (1,25-dihydroxycholecalciferol, 1,25(OH)D). The conversion of calcifediol to calcitriol is catalyzed by the enzyme 25-hydroxyvitamin D 1-alpha-hydroxylase, which is the product of the "CYP27B1" human gene. The activity of CYP27B1 is increased by parathyroid hormone, and also by low calcium or phosphate. Following the final converting step in the kidney, calcitriol is released into the circulation. By binding to vitamin D-binding protein, calcitriol is transported throughout the body, including to the classical target organs of intestine, kidney and bone. Calcitriol is the

pos: Vegetarian and vegan dog diet of vitamin D) to cholecalciferol (inactive form of vitamin D) following exposure to UV light from the sun. Cholecalciferol is then converted to calcidiol in the liver before further hydroxylated to calcitriol, the active form of vitamin D, in the kidney. However, the conversion of provitamin D to cholecalciferol is significantly lower in dogs than other mammals, and is not sufficient to maintain an adequate vitamin D status. Thus, dogs depend on dietary sources of vitamin D to meet their nutrient requirement. In the diet, there are two forms of vitamin D – cholecalciferol (vitamin D) from mainly animal sources,

pos: Hypervitaminosis D active form of vitamin D, calcitriol, are inversely correlated with coronary calcification. Moreover, the active vitamin D analog, alfacalcidol, seems to protect patients from developing vascular calcification. Serum vitamin D has been found to correlate with calcified atherosclerotic plaque in African Americans as they have higher active serum vitamin D levels compared to Euro-Americans. Higher levels of calcidiol positively correlate with aorta and carotid calcified atherosclerotic plaque in African Americans but not with coronary plaque, whereas individuals of European descent have an opposite, negative association. There are racial differences in the association of coronary calcified plaque in that there is

pos: Vitamin D deficiency levels decline during stays in intensive care. Vitamin D3 (cholecalciferol) or calcitriol given orally may reduce the mortality rate without significant adverse effects. The serum concentration of 25(OH)D is typically used to determine vitamin D status. Most vitamin D is converted to 25(OH)D in the serum, giving an accurate picture of vitamin D status. The level of serum 1,25(OH)D is not usually used to determine vitamin D status because it often is regulated by other hormones in the body such as parathyroid hormone. The levels of 1,25(OH)D can remain normal even when a person may be vitamin D deficient. Serum

pos: Chronic kidney disease-mineral and bone disorder the "bone pathology" associated with CKD. Thus, renal osteodystrophy is currently considered "one" measure of the skeletal component of the systemic disorder of CKD–MBD that is quantifiable by histomorphometry of bone biopsy. New guidelines have been recently released It is well-known that as kidney function declines, there is a progressive deterioration in mineral homeostasis, with a disruption of normal serum and tissue concentrations of phosphorus and calcium, and changes in circulating levels of hormones. These include parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH) vitamin D; calcidiol), 1,25-dihydroxyvitamin D (1,25(OH)2 vitamin D; calcitriol), and other vitamin D metabolites, fibroblast growth factor 23

pos: Vitamin D Circulating calcifediol may then be converted into calcitriol, the biologically active form of vitamin D, in the kidneys. Whether it is made in the skin or ingested, Vitamin D is hydroxylated in the liver at position 25 (upper right of the molecule) to form 25-hydroxycholecalciferol (calcifediol or 25(OH)D). This reaction is catalyzed by the microsomal enzyme vitamin D 25-hydroxylase, the product of the "CYP2R1" human gene, and expressed by hepatocytes. Once made, the product is released into the plasma, where it is bound to an α-globulin carrier protein named the vitamin D-binding protein. Calcifediol is transported to the proximal tubules

pos: CYP2R1 proline for a leucine residue at codon 99 eliminates the enzyme activity and is associated with low circulating levels of 25-hydroxyvitamin D and classic symptoms of vitamin D deficiency. The gene product which it encodes, vitamin D 25-hydroxylase, has therefore been proposed as the key enzyme in the conversion of cholecalciferol (vitamin D) to calcidiol. Calcidiol is subsequently converted by the action of 25-hydroxyvitamin D3 1-alpha-hydroxylase to calcitriol, the active form of vitamin D that binds to the vitamin D receptor (VDR) which mediates most of the physiological actions of the vitamin. Model organisms have been used in the study

pos: Michael F. Holick Michael F. Holick 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. He is a professor of medicine at the Boston University Medical Center and editor-in-chief of the journal "Clinical Laboratory". After earning a Ph.D. degree in biochemistry, a medical degree, and completing a research postdoctoral fellowship at the University of Wisconsin–Madison, Holick completed a

pos: Michael F. Holick the Van Slyke Award from American Association for Clinical Chemistry, the Linus Pauling Prize In Human Nutrition, the Delbert A Fisher Research Scholar Award from the Endocrine Society, and the American College of Nutrition's Communication Media Award. Michael F. Holick 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. He is a professor of medicine

pos: Calcium metabolism blood. Calcitriol is a cholesterol derivative. Under the influence of ultraviolet light on the skin, cholesterol is converted to previtamin D which spontaneously isomerizes to vitamin D (or cholecaliferol). It is then converted from cholecaliferol to calcifediol in the liver. Under the influence of parathyroid hormone, the kidneys convert calcifediol into the active hormone calcitriol, which acts on the epithelial cells (enterocytes) lining the small intestine to increase the rate of absorption of calcium from the intestinal contents. In short the cycle is following: Low PTH levels in the blood (which occur under physiological conditions when the plasma ionized calcium

pos: CYP24A1 the gene may also be found in people with renal stones. CYP24A1 Cytochrome P450 family 24 subfamily A member 1 (abbreviated CYP24A1) is a member of the cytochrome P450 superfamily of enzymes encoded by the "CYP24A1" gene. It is a mitochondrial monooxygenase which catalyzes reactions including 24-hydroxylation of calcitriol (1,25-dihydroxyvitamin D). It has also been identified as vitamin D3 24-hydroxylase.() CYP24A1 is an enzyme expressed in the mitochondrion of humans and other species. It catalyzes hydroxylation reactions which lead to the degradation of 1,25-dihydroxyvitamin D, the physiologically active form of vitamin D. Hydroxylation of the side chain produces calcitroic acid

pos: CYP24A1 CYP24A1 Cytochrome P450 family 24 subfamily A member 1 (abbreviated CYP24A1) is a member of the cytochrome P450 superfamily of enzymes encoded by the "CYP24A1" gene. It is a mitochondrial monooxygenase which catalyzes reactions including 24-hydroxylation of calcitriol (1,25-dihydroxyvitamin D). It has also been identified as vitamin D3 24-hydroxylase.() CYP24A1 is an enzyme expressed in the mitochondrion of humans and other species. It catalyzes hydroxylation reactions which lead to the degradation of 1,25-dihydroxyvitamin D, the physiologically active form of vitamin D. Hydroxylation of the side chain produces calcitroic acid and other metabolites which are excreted in bile. CYP24A1 was identified

pos: Eldecalcitol for their regulatory effects on calcium metabolism with the purpose of treating osteoporosis, a skeletal disease associated with low bone mass and deterioration of bone tissue. Vitamin D is imperative for absorption of calcium to maintain bone strength. Eldecalcitol is an orally administered drug to patients, which binds to vitamin D receptors and binding protein for the goal of achieving greater specificity to bind calcium for its absorption. This greater affinity is 2.7-fold that of the active vitamin D form of calcitriol. Eldecalcitol is readily absorbed into the body, with a long elimination half-life of over eight hours, reaching maximum

pos: Vitamin D-binding protein multifunctional protein found in plasma, ascitic fluid, cerebrospinal fluid and on the surface of many cell types. It is able to bind the various forms of vitamin D including ergocalciferol (vitamin D) and cholecalciferol (vitamin D), the 25-hydroxylated forms (calcifediol), and the active hormonal product, 1,25-dihydroxyvitamin D (calcitriol). The major proportion of vitamin D in blood is bound to this protein. It transports vitamin D metabolites between skin, liver and kidney, and then on to the various target tissues. As Gc protein-derived macrophage activating factor it is a Macrophage Activating Factor (MAF) that has been tested for use as a

pos: Vitamin D the various forms of vitamin D are secosteroids, i.e., steroids in which one of the bonds in the steroid rings is broken. The structural difference between vitamin D and vitamin D is the side chain of D contains a double bond between carbons 22 and 23, and a methyl group on carbon 24. The active vitamin D metabolite calcitriol mediates its biological effects by binding to the vitamin D receptor (VDR), which is principally located in the nuclei of target cells. The binding of calcitriol to the VDR allows the VDR to act as a transcription factor that modulates the

neg: 24,25-Dihydroxycholecalciferol of 25-hydroxyvitamin D which is destined for excretion. It is not known whether the compound might also have some physiologically significant activity. Some evidence of a possible receptor has been obtained. 24,25-Dihydroxycholecalciferol 24,25-Dihydroxycholecalciferol, also known as 24,25-dihydroxyvitamin D and (24"")-hydroxycalcidiol (abbreviated as 24(R),25-(OH)D), is a compound which is closely related to 1,25-dihydroxyvitamin D, the active form of vitamin D, but like vitamin D itself and 25-hydroxyvitamin D is inactive as a hormone both "in vitro" and "in vivo". It was identified by Michael F. Holick. 24,25-dihydroxyvitamin D is formed from 25-hydroxyvitamin D by the action of P450cc24 (25-hydroxyvitamin D3-24-hydroxylase), which

neg: Parathyroid hormone of phosphate is not as dependent on vitamin D as is that of calcium. The end result of PTH release is a small net drop in the serum concentration of phosphate. PTH upregulates the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol, the major circulating form of inactive vitamin D, into 1,25-dihydroxycholecalciferol, the active form of vitamin D, in the kidney. Secretion of parathyroid hormone is determined chiefly by serum ionized calcium concentration through negative feedback. Parathyroid cells express calcium-sensing receptors on the cell surface. PTH is secreted when [Ca] is decreased (calcitonin is secreted when serum calcium levels are elevated).

neg: 24,25-Dihydroxycholecalciferol 24,25-Dihydroxycholecalciferol 24,25-Dihydroxycholecalciferol, also known as 24,25-dihydroxyvitamin D and (24"")-hydroxycalcidiol (abbreviated as 24(R),25-(OH)D), is a compound which is closely related to 1,25-dihydroxyvitamin D, the active form of vitamin D, but like vitamin D itself and 25-hydroxyvitamin D is inactive as a hormone both "in vitro" and "in vivo". It was identified by Michael F. Holick. 24,25-dihydroxyvitamin D is formed from 25-hydroxyvitamin D by the action of P450cc24 (25-hydroxyvitamin D3-24-hydroxylase), which appears to be "a multicatalytic enzyme catalyzing most, if not all, of the reactions in the C-24/C-23 pathway of 25-OH-D3 metabolism." It has been proposed that 24,25-dihydroxyvitamin D is a metabolite

neg: Vitamin D and neurology food sources including milk and fish. These two forms of vitamin D are metabolized in the liver and stored as 25-hydroxyvitamin D. Before biological use, the storage form must be converted into an active form. One common active form is 1,25 dihydroxyvitamin D. The term "vitamin D" in this article, refers to group of molecules including cholecalciferol, ergocalciferol, 25-hydroxyvitamin D, and the active forms. The role of vitamin D is best characterized as enabling calcium absorption and regulating calcium homeostasis. Vitamin D also play a role in phosphate absorption. Hypovitaminosis D is described as any deficiency of vitamin D. A

neg: Paricalcitol Paricalcitol Paricalcitol (chemically it is 19-nor-1,25-(OH)-vitamin D. Marketed by Abbott Laboratories under the trade name Zemplar) is a drug used for the prevention and treatment of secondary hyperparathyroidism (excessive secretion of parathyroid hormone) associated with chronic renal failure. It is an analog of 1,25-dihydroxyergocalciferol, the active form of vitamin D (ergocalciferol). Its primary use in medicine is in the treatment of secondary hyperparathyroidism associated with chronic kidney disease. In three placebo-controlled studies, chronic renal failure patients treated with paricalcitol achieved a mean parathyroid hormone (PTH) reduction of 30% in six weeks. Additionally there was no difference in incidence of hypercalcemia

neg: Paricalcitol every other day (3 times per week). Paricalcitol Paricalcitol (chemically it is 19-nor-1,25-(OH)-vitamin D. Marketed by Abbott Laboratories under the trade name Zemplar) is a drug used for the prevention and treatment of secondary hyperparathyroidism (excessive secretion of parathyroid hormone) associated with chronic renal failure. It is an analog of 1,25-dihydroxyergocalciferol, the active form of vitamin D (ergocalciferol). Its primary use in medicine is in the treatment of secondary hyperparathyroidism associated with chronic kidney disease. In three placebo-controlled studies, chronic renal failure patients treated with paricalcitol achieved a mean parathyroid hormone (PTH) reduction of 30% in six weeks. Additionally there

neg: Michael F. Holick Vitamin D has been called extreme, even speculating that the extinction of the dinosaurs could be caused by a lack of it in the reduced sunlight. As a graduate student, he identified the major circulating form of vitamin D, 25-hydroxyvitamin D3, which is the vitamin D metabolite that is measured by physicians worldwide to determine a patient's vitamin D status. He also identified the active form of vitamin D, 1,25-dihydroxyvitamin D3, as well as other metabolites including 24,25-dihydroxyvitamin D3, 1,24,25-trihydroxyvitamin D3 and 25,26-dihydroxyvitamin D3. As a fellow, he participated in the first chemical synthesis of 1,25-dihydroxyvitamin D3 and 1α-hydroxyvitamin D3

neg: Vitamin A retinol), which is an important hormone-like growth factor for epithelial and other cells. In foods of animal origin, the major form of vitamin A is an ester, primarily retinyl palmitate, which is converted to retinol (chemically an alcohol) in the small intestine. The retinol form functions as a storage form of the vitamin, and can be converted to and from its visually active aldehyde form, retinal. All forms of vitamin A have a beta-ionone ring to which an isoprenoid chain is attached, called a "retinyl group". Both structural features are essential for vitamin activity. The orange pigment of carrots (beta-carotene)

neg: Hyperparathyroidism most common causes are vitamin D deficiency (caused by lack of sunlight, diet or malabsorption) and chronic kidney failure. Lack of vitamin D leads to reduced calcium absorption by the intestine leading to hypocalcemia and increased parathyroid hormone secretion. This increases bone resorption. In chronic kidney failure the problem is more specifically failure to convert vitamin D to its active form in the kidney. The bone disease in secondary hyperparathyroidism caused by kidney failure is termed renal osteodystrophy. Tertiary hyperparathyroidism is seen in patients with long-term secondary hyperparathyroidism, which eventually leads to hyperplasia of the parathyroid glands and a loss

neg: Retinal retinal, retinal is the precursor of the other forms of vitamin A. Retinal is interconvertible with retinol (ROL), the transport and storage form of vitamin A catalyzed by retinol dehydrogenases (RDHs) and alcohol dehydrogenases (ADHs). Retinol is called vitamin A alcohol, or more often, simply vitamin A. Retinal can also be oxidized to retinoic acid (RA) catalyzed by retinal dehydrogenases also known as retinaldehyde dehydrogenases (RALDHs) as well as retinal oxidases. Retinoic acid, sometimes called vitamin A acid, is an important signaling molecule and hormone in vertebrate animals. Vision begins with the photoisomerization of retinal. When the 11-"cis"-retinal chromophore absorbs

neg: Vitamin D a hormone involved in morphogenesis. Vitamin D Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, and multiple other biological effects. In humans, the most important compounds in this group are vitamin D (also known as cholecalciferol) and vitamin D (ergocalciferol). Cholecalciferol and ergocalciferol can be ingested from the diet and from supplements. Only a few foods contain vitamin D. The major natural source of the vitamin is synthesis of cholecalciferol in the skin from cholesterol through a chemical reaction that is dependent on sun exposure (specifically UVB radiation). Dietary recommendations

neg: Hyperparathyroidism vitamin D from cholesterol. The resulting hypovitaminosis D is usually due to a partial combination of both factors. Vitamin D (or cholecalciferol) is converted to 25-hydroxyvitamin D (or calcidiol) by the liver, from where it is transported via the circulation to the kidneys where it is converted into the active hormone, 1,25 dihydroxyvitamin D. Thus a third cause of secondary hyperparathyroidism is chronic kidney disease. Here the ability to manufacture 1,25 dihydroxyvitamin D is compromised, resulting in hypocalcemia. The gold standard of diagnosis is the parathyroid immunoassay. Once an elevated Parathyroid hormone has been confirmed, the goal of diagnosis is

neg: VDRE naturally occurring sequences. The VDR is widely distributed in tissues, and is not restricted to those tissues considered the classic targets of vitamin D. The VDR upon binding to 1,25(OH)2D heterodimerizes with other nuclear hormone receptors, in particular the family of retinoid X receptors. This complex then binds to special DNA sequences called vitamin D response elements (VDRE) in the promoters of genes which it regulates. A variety of additional proteins called coactivators complex with the activated VDR/RXR heterodimers either to form a bridge from the VDR/RXR complex binding to the VDRE to the proteins responsible for transcription such as

neg: Vitamin D deficiency the metabolism of vitamin D, causing a deficiency. Some types of liver diseases and kidney diseases can decrease vitamin D production leading to a deficiency. The liver is required to transform vitamin D into 25-hydroxyvitamin D. This is an inactive metabolite of vitamin D but is a necessary precursor (building block) to create the active form of vitamin D. In liver disease, the 25-hydroxyvitamin D may not be formed, leading to a vitamin D deficiency. The kidneys are responsible for converting 25-hydroxyvitamin D to 1,25-hydroxyvitamin D. This is the active form of vitamin D in the body. Kidney disease often

neg: Cathelicidin were originally found in neutrophils, but have since been found in many other cells including epithelial cells and macrophages after activation by bacteria, viruses, fungi, or the hormone 1,25-D, which is the hormonally active form of vitamin D. The protein encoded by the human cathelicidin gene, "CAMP", is cleaved into the LL-37 peptide, which has several immunological functions. Cathelicidins range in size from 12 to 80 amino acid residues and have a wide range of structures. Most cathelicidins are linear peptides with 23-37 amino acid residues, and fold into amphipathic α-helices. Additionally cathelicidins may also be small-sized molecules (12-18 residues)

neg: Anthony W. Norman Anthony W. Norman Anthony W. Norman is a distinguished professor emeritus of biochemistry and biomedical sciences at the University of California, Riverside and one of the world's foremost experts on vitamin D. Formally stated, Norman's research is the "mechanism of action of the steroid hormone 1,25(OH)2-vitamin D3; vitamin D structure-function relationships, actions of the vitamin D receptor (VDR)." In 1967, Norman's lab discovered that vitamin D is converted into a steroid hormone by the body. In 1969 he determined that vitamin D receptors (VDR) were present in the intestine. In 1971 the Norman laboratory reported the chemical structure of the

neg: Vitamin D been destroyed. The modified oil cured the sick dogs, so McCollum concluded the factor in cod liver oil which cured rickets was distinct from vitamin A. He called it vitamin D because it was the fourth vitamin to be named. It was not initially realized that, unlike other vitamins, vitamin D can be synthesised by humans through exposure to UV light. In 1925, it was established that when 7-dehydrocholesterol is irradiated with light, a form of a fat-soluble vitamin is produced (now known as D). Alfred Fabian Hess stated: "Light equals vitamin D." Adolf Windaus, at the University of Göttingen

neg: Vitamin D maintain skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain serum calcium levels. Vitamin D deficiency can result in lower bone mineral density and an increased risk of reduced bone density (osteoporosis) or bone fracture because a lack of vitamin D alters mineral metabolism in the body. Thus, vitamin D is also critical for bone remodeling through its role as a potent stimulator of bone resorption. The VDR regulates cell proliferation and differentiation. Vitamin D

neg: 7-Dehydrocholesterol skin to meet the body's vitamin D requirements. 7-Dehydrocholesterol 7-Dehydrocholesterol (7-DHC) is a zoosterol that functions in the serum as a cholesterol precursor, and is converted to vitamin D in the skin, therefore functioning as provitamin-D. The presence of this compound in human skin enables humans to manufacture vitamin D (cholecalciferol) from ultraviolet rays in the sun light, via an intermediate isomer pre-vitamin D. It is also found in the milk of several mammalian species. In insects it is a precursor for the hormone ecdysone, required for reaching adulthood. It was discovered by Nobel-laureate organic chemist Adolf Windaus. The skin

neg: Vitamin D and neurology neurons. Hypovitaminosis D has also been associated with many other conditions, including both neurological and non neurological conditions. These include but are not limited to autism, diabetes, and osteoporosis. Hypovitaminosis D has been associated with many neurological conditions. However, an actual mechanism of attack for each of the conditions has yet to be solidified. Many researchers have questioned whether the depletion of vitamin D actually causes these disorders or if vitamin D is a symptom of these disorders. Future research is needed to fully answer these questions. Vitamin D and neurology Vitamin D is a steroid hormone that plays a

neg: Vitamin D itself is auto-regulated in a negative feedback cycle, and is also affected by parathyroid hormone, fibroblast growth factor 23, cytokines, calcium, and phosphate. Vitamin D overdose causes hypercalcemia, which is a strong indication of vitamin D toxicity – this can be noted with an increase in urination and thirst. If hypercalcemia is not treated, it results in excess deposits of calcium in soft tissues and organs such as the kidneys, liver, and heart, resulting in pain and organ damage. The main symptoms of vitamin D overdose which are those of hypercalcemia including anorexia, nausea, and vomiting. These may be followed

neg: Vitamin D a person's vitamin D is taken by mouth, as sun exposure in the population is variable and recommendations about the amount of sun exposure that is safe are uncertain in view of the skin cancer risk. Vitamin D from the diet or skin synthesis is biologically inactive; enzymatic conversion (hydroxylation) in the liver and kidney is required for activation. As vitamin D can be synthesized in adequate amounts by most mammals exposed to sufficient sunlight, it is not an essential dietary factor, and so not technically a vitamin. Instead it could be considered a hormone, with activation of the vitamin

neg: Secondary hyperparathyroidism form, and they do not adequately excrete phosphate. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes lead to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from malabsorption (chronic pancreatitis, small bowel disease, malabsorption-dependent bariatric surgery) in that the fat-soluble vitamin D can not get reabsorbed. This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum calcium levels. The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D. It is usually seen in cases of chronic

neg: Vitamin D and neurology Vitamin D and neurology Vitamin D is a steroid hormone that plays a vital role in calcium and phosphate absorption. In recent studies, several associations between low levels of vitamin D, or hypovitaminosis D, and neuropsychiatric disorders have begun to surface. These disorders include, but are not limited to: Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, schizophrenia, and autism. Vitamin D is mainly found in the body in two forms: vitamin D3 and vitamin D2. Vitamin D3, or cholecalciferol, is formed in the skin after exposure to sunlight or ultra violet radiation. Vitamin D2, or ergocalciferol, is obtained from various

neg: 7-Dehydrocholesterol 7-Dehydrocholesterol 7-Dehydrocholesterol (7-DHC) is a zoosterol that functions in the serum as a cholesterol precursor, and is converted to vitamin D in the skin, therefore functioning as provitamin-D. The presence of this compound in human skin enables humans to manufacture vitamin D (cholecalciferol) from ultraviolet rays in the sun light, via an intermediate isomer pre-vitamin D. It is also found in the milk of several mammalian species. In insects it is a precursor for the hormone ecdysone, required for reaching adulthood. It was discovered by Nobel-laureate organic chemist Adolf Windaus. The skin consists of two primary layers: an inner layer,

neg: Vitamin D gene expression of transport proteins (such as TRPV6 and calbindin), which are involved in calcium absorption in the intestine. The vitamin D receptor belongs to the nuclear receptor superfamily of steroid/thyroid hormone receptors, and VDRs are expressed by cells in most organs, including the brain, heart, skin, gonads, prostate, and breast. VDR activation in the intestine, bone, kidney, and parathyroid gland cells leads to the maintenance of calcium and phosphorus levels in the blood (with the assistance of parathyroid hormone and calcitonin) and to the maintenance of bone content. One of the most important roles of vitamin D is to

neg: Calcitriol receptor "VDR" gene. Glucocorticoids are known to decrease expression of VDR, which is expressed in most tissues of the body and regulate intestinal transport of calcium, iron and other minerals. This gene encodes the nuclear hormone receptor for vitamin D. This receptor also functions as a receptor for the secondary bile acid lithocholic acid. The receptor belongs to the family of trans-acting transcriptional regulatory factors and shows similarity of sequence to the steroid and thyroid hormone receptors. Downstream targets of this nuclear hormone receptor are involved principally in mineral metabolism though the receptor regulates a variety of other metabolic pathways, such

neg: Immune system levels with age is partially responsible for weakened immune responses in aging individuals. Conversely, some hormones are regulated by the immune system, notably thyroid hormone activity. The age-related decline in immune function is also related to decreasing vitamin D levels in the elderly. As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels. This means that they get less sun and therefore produce less cholecalciferol via UVB radiation. Second, as a person ages the skin becomes less adept at producing vitamin D. The immune system is affected

neg: T helper 17 cell HIV infection (Gosselin et al. J Immunol 2010). The active form of vitamin D (1,25-Dihydroxyvitamin D3) has been found to 'severely impair' production of the IL-17 and IL-17F cytokines by Th17 cells. Thus, active form of vitamin D is a direct inhibitor for Th17 differentiation. In this way, oral administration of vitamin D3 was proposed to be a promising tool for the treatment of Th17-mediated diseases. In young patients with asthma 1,25-Dihydroxyvitamin D3-treated dendritic cells significantly reduced the percentage of Th17 cells, as well as IL-17 production. T helper 17 cell T helper 17 cells (T17) are a subset of

neg: Chronic kidney disease-mineral and bone disorder (FGF-23), and growth hormone. Beginning in CKD stage 3, the ability of the kidneys to appropriately excrete a phosphate load is diminished, leading to hyperphosphatemia, elevated PTH (secondary hyperparathyroidism), and decreased 1,25(OH)2 vitamin D with associated elevations in the levels of FGF-23. The conversion of 25(OH) vitamin D to 1,25(OH)2 vitamin D is impaired, reducing intestinal calcium absorption and increasing PTH. The kidney fails to respond adequately to PTH, which normally promotes phosphaturia and calcium reabsorption, or to FGF-23, which also enhances phosphate excretion. In addition, there is evidence at the tissue level of a downregulation of vitamin D receptor

neg: CYP2R1 CYP2R1 Vitamin D 25-hydroxylase also known as cytochrome P450 2R1 is an enzyme that in humans is encoded by the "CYP2R1" gene. Vitamin D 25-hydroxylase is a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. Found in the liver, this enzyme is a microsomal vitamin D hydroxylase that converts vitamin D into 25-hydroxyvitamin D (calcidiol), which is the major circulatory form of the vitamin. An inherited mutation in the "CYP2R1" gene which results in the substitution of a

neg: Retinoic acid receptor beta Retinoic acid receptor beta Retinoic acid receptor beta (RAR-beta), also known as NR1B2 (nuclear receptor subfamily 1, group B, member 2) is a nuclear receptor that in humans is encoded by the "RARB" gene. This gene encodes retinoic acid receptor beta, a member of the thyroid-steroid hormone receptor superfamily of nuclear transcriptional regulators. This receptor localizes to the cytoplasm and to subnuclear compartments. It binds retinoic acid, the biologically active form of vitamin A which mediates cellular signalling in embryonic morphogenesis, cell growth and differentiation. It is thought that this protein limits growth of many cell types by regulating gene

neg: Vitamin D deficiency Vitamin D deficiency Vitamin D deficiency, or hypovitaminosis D, most commonly results from inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D, disorders limiting vitamin D absorption, and conditions impairing vitamin D conversion into active metabolites—including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone softening diseases such as rickets in children. It can also worsen osteomalacia and osteoporosis in adults, leading to an increased risk of bone fractures. Muscle weakness is also a common symptom of vitamin D deficiency,

neg: Hypervitaminosis D D toxicity (starting at a plasmatic concentration of ≈750 nmol/L) propose that: All of which affect gene transcription and overwhelm the vitamin D signal transduction process, leading to vitamin D toxicity. Evidence suggests that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages. This raises questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk as it may be causing vascular calcification. Calcifediol is implicated in the etiology of atherosclerosis, especially in non-Caucasians. The levels of the

neg: Bone remodeling include the action of several hormones, including parathyroid hormone (PTH), vitamin D, growth hormone, steroids, and calcitonin, as well as several bone marrow-derived membrane and soluble cytokines and growth factors (ex. M-CSF, RANKL, VEGF, IL-6 family...). It is in this way that the body is able to maintain proper levels of calcium required for physiological processes. Thus bone remodeling is not just occasional "repair of bone damage" but rather an active, continual process that is always happening in a healthy body. Subsequent to appropriate signaling, osteoclasts move to resorb the surface of the bone, followed by deposition of bone by

neg: CYP24A1 in the early 1970s and was first thought to be involved in vitamin D metabolism as the renal 25-hydroxyvitamin D3-24-hydroxylase, modifying calcifediol (25-hydroxyvitamin D) to produce 24,25-dihydroxycholecalciferol (24,25-dihydroxyvitamin D). Subsequent studies using recombinant CYP24A1 showed that it could also catalyze multiple other hydroxylation reactions at the side chain carbons known as C-24 and C-23 in both 25-OH-D and the active hormonal form, 1,25-(OH)D. It is now considered responsible for the entire five-step, 24-oxidation pathway from 1,25-(OH)D producing calcitroic acid. CYP24A1 also is able to catalyse another pathway which starts with 23-hydroxylation of 1,25-(OH)D and culminates in 1,25-(OH)D-26,23-lactone. The side chains

neg: Vitamin A as heterodimers with retinoid "X" receptors (RXRs). RAR and RXR must dimerize before they can bind to the DNA. RAR will form a heterodimer with RXR (RAR-RXR), but it does not readily form a homodimer (RAR-RAR). RXR, on the other hand, may form a homodimer (RXR-RXR) and will form heterodimers with many other nuclear receptors as well, including the thyroid hormone receptor (RXR-TR), the Vitamin D receptor (RXR-VDR), the peroxisome proliferator-activated receptor (RXR-PPAR) and the liver "X" receptor (RXR-LXR). The RAR-RXR heterodimer recognizes retinoic acid response elements (RAREs) on the DNA whereas the RXR-RXR homodimer recognizes retinoid "X" response elements

neg: Women's Health Initiative abuse, mental illness, or cognitive impairment), or concurrent enrollment in another randomized controlled clinical trial. For the CT, a partial factorial study design was utilized for the investigation of three overlapping interventions (dietary modification, hormone therapy, and calcium/vitamin D supplementation), as this would provide considerable cost efficiencies. Willing study-eligible women were asked to join either the hormone therapy (HT trial), the dietary modification (DM) trial, or both. After one year, willing and eligible CT participants were also asked to join the calcium/vitamin D trial (CaD). Recruitment goals for the HT, DM, and CaD components of the CT were 27,500, 48,000,

neg: RANKL fractures and spinal cord compression. However, survival rates for both clinical groups were comparable. Hormone receptor positive breast cancer patients have a significant increased risk of complications such as osteopenia and osteoporosis. About two out of every three breast cancer patients are hormone receptor positive. In the past several years, denosumab has been used in clinical trials, primarily because a large population is affected by bone complication among those who have breast cancer. 252 patients enlisted in the HALT-BC clinical trial (also known as NCT00089661). In addition to receiving vitamin D and calcium supplements, half of the patients were randomly

neg: Hypervitaminosis D reasons as well as environmental ones. Possible ethnic differences in physiological pathways for ingested vitamin D, such as the Inuit, may confound across the board recommendations for vitamin D levels. Inuit compensate for lower production of vitamin D by converting more of this vitamin to its most active form. A Toronto study of young Canadians of diverse ancestry applied a standard of serum 25(OH)D levels that was significantly higher than official recommendations. These levels were described to be 75 nmol/L as "optimal", between 75 nmol/L and 50 nmol/L as "insufficient" and < 50 nmol/L as "deficient". 22% of individuals of

neg: Hypoparathyroidism fact that there is no exact form of the hormone that can be administered as replacement. However teriparatide, brand name Forteo, a biosimilar peptide to parathyroid hormone, may be given by injection. Calcium replacement or vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and chronic kidney disease. The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well

neg: Edible mushroom twice the U.S. Food and Drug Administration's daily recommendation of vitamin D, and 5 minutes of UV light exposure after harvesting made a serving of mushrooms contain four times the FDA's daily recommendation of vitamin D. Analysis also demonstrated that natural sunlight produced vitamin D. The ergocalciferol, vitamin D, in UV-irradiated mushrooms is not the same form of vitamin D as is produced by UV-irradiation of human skin or animal skin, fur, or feathers (cholecalciferol, vitamin D). Although vitamin D clearly has vitamin D activity in humans and is widely used in food fortification and in nutritional supplements, vitamin D

neg: Calcium supplement citrate, calcium gluconate, calcium lactate and calcium phosphate. Vitamin D is added to some calcium supplements. Proper vitamin D status is important because vitamin D is converted to a hormone in the body, which then induces the synthesis of intestinal proteins responsible for calcium absorption. For U.S. dietary supplement and food labeling purposes the amount in a serving is expressed in milligrams and as a percent of Daily Value (%DV). The weight is for the calcium part of the compound - for example, calcium citrate - in the supplement. For calcium labeling purposes 100% of the Daily Value was 1000

neg: Vitamin D deficiency thought to correlated with cardiovascular disease, type 1 diabetes, type 2 diabetes, and some cancers. Review studies have also seen associations between vitamin D deficiency and preeclampsia. Vitamin D deficiency Vitamin D deficiency, or hypovitaminosis D, most commonly results from inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D, disorders limiting vitamin D absorption, and conditions impairing vitamin D conversion into active metabolites—including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone softening diseases such as rickets in children. It

neg: Anti-Müllerian hormone AMH regulation. The AMH gene promoter contains a vitamin D response element that may cause vitamin D status to influence serum AMH levels. Women with levels of Vitamin D of 267.8 ± 66.4 nmol/L show a 4 times better success rate with IVF procedure than those with low levels of 104.3 ± 21 nmol/L. Vitamin D deficiency should be considered when serum AMH levels are obtained for diagnosis. In women with cancer, radiation therapy and chemotherapy can damage the ovarian reserve. In such cases, a pre-treatment AMH is useful in predicting the long-term post-chemotherapy loss of ovarian function, which may

neg: Rickets of ultraviolet light therapy and medicine. Recommendations are for 400 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance. Sufficient vitamin D levels can also be achieved through dietary supplementation and/or exposure to sunlight. Vitamin D (cholecalciferol) is the preferred form since it is more readily absorbed than vitamin D. Most dermatologists recommend vitamin D supplementation as an alternative to unprotected ultraviolet

neg: Secondary hyperparathyroidism Secondary hyperparathyroidism Secondary hyperparathyroidism (SHPT) refers to the excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and associated hyperplasia of the glands. This disorder is especially seen in patients with chronic kidney failure. It is often—although not consistently—abbreviated as SHPT in medical literature. Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on the blood, immune system, and neurological system. Chronic kidney failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active

neg: Cholecalciferol consensus is that supplementing levels is not beneficial. It is thought that tuberculosis may result in lower levels. It, however, is not entirely clear how the two are related. Cholecalciferol is one of the five forms of vitamin D. Cholecalciferol is a secosteroid, that is, a steroid molecule with one ring open. By itself cholecalciferol is inactive. It is converted to its active form by two hydroxylations: the first in the liver, by CYP2R1 or CYP27A1, to form 25-hydroxycholecalciferol (calcifediol, 25-OH vitamin D). The second hydroxylation occurs mainly in the kidney through the action of CYP27B1 to convert 25-OH vitamin

neg: Vitamin K calcification of arteries and other soft tissues. Chemically, the vitamin K family comprises 2-methyl-1,4-naphthoquinone (3-) derivatives. Vitamin K includes two natural vitamers: vitamin K and vitamin K. Vitamin K, in turn, consists of a number of related chemical subtypes, with differing lengths of carbon side chains made of isoprenoid groups of atoms. Vitamin K, also known as phylloquinone, is made by plants, and is found in highest amounts in green leafy vegetables because it is directly involved in photosynthesis. It may be thought of as the plant form of vitamin K. It is active as a vitamin in animals and

neg: Calcitonin family. Calcitonin is formed by the proteolytic cleavage of a larger prepropeptide, which is the product of the CALC1 gene (). It is functionally an antagonist with PTH and Vitamin D3.The CALC1 gene belongs to a superfamily of related protein hormone precursors including islet amyloid precursor protein, calcitonin gene-related peptide, and the precursor of adrenomedullin. Secretion of calcitonin is stimulated by: The hormone participates in calcium (Ca) and phosphorus metabolism. In many ways, calcitonin counteracts parathyroid hormone (PTH) and vitamin D More specifically, calcitonin lowers blood Ca levels in two ways: High concentrations of calcitonin may be able to increase

neg: Damaraland mole-rat drink, obtaining all their water from their food, which is also an important source of minerals. Unlike most other mammals, they can effectively metabolise these minerals without access to vitamin D, which they lack because they are normally never exposed to sunlight. The basal metabolic rate of Damaraland mole rats is also unusually low for mammals of their size, at just 0.66 cm O / g · h. Despite living in an entirely subterranean environment, Damaraland mole-rats exhibit circadian rhythms, and are active primarily during the day. Their levels of the hormone melatonin can be altered by artificially changing the

neg: Vitamin D and neurology regulating 900 genes within our bodies, as well as how this pair interacts genetically. For example genes can be upregulated or downregulated when the highly active form of vitamin D, 1, 25-alpha dihydroxyvitamin D3 binds to the VDR on chromosomal regions of gene expression that manage the balance or ratio between differentiating immune cells into Th1 and Th2 T cell proteins Seizures are disturbances in brain activities where neurons fire abnormally. Epilepsy is a condition in which a person experiences repeated seizures. In one small pilot study (Christiansen, 1974, BMJ), vitamin D supplementation, but not placebo treatment was associated with

neg: Calcium Conversely, inadequate calcium or vitamin D intakes may result in hypocalcaemia, often caused also by inadequate secretion of parathyroid hormone or defective PTH receptors in cells. Symptoms include neuromuscular excitability, which potentially causes tetany and disruption of conductivity in cardiac tissue. As calcium is heavily involved in bone manufacture, many bone diseases can be traced to problems with the organic matrix or the hydroxyapatite in molecular structure or organisation. For example, osteoporosis is a reduction in mineral content of bone per unit volume, and can be treated by supplementation of calcium, vitamin D, and biphosphates. Calcium supplements may benefit the

neg: Hormone receptor Hormone receptor A hormone receptor is a receptor molecule that binds to a specific hormone. Hormone receptors are a wide family of proteins made up of receptors for thyroid and steroid hormones, retinoids and Vitamin D, and a variety of other receptors for various ligands, such as fatty acids and prostaglandins. There are two main classes of hormone receptors. Receptors for peptide hormones tend to be cell surface receptors built into the plasma membrane of cells and are thus referred to as trans membrane receptors. An example of this is insulin. Receptors for steroid hormones are usually found within the

neg: Disorders of calcium metabolism be life-threatening. Hypocalcemia can be parathyroid related or vitamin D related. Parathyroid related hypocalcemia includes post-surgical hypoparathyroidism, inherited hypoparathyroidism, pseudohypoparathyroidism, and pseudo-pseudohypoparathyroidism. Post-surgical hypoparathyroidism is the most common form, and can be temporary (due to suppression of tissue after removal of a malfunctioning gland) or permanent, if all parathyroid tissue has been removed. Inherited hypoparathyroidism is rare and is due to a mutation in the calcium sensing receptor. Pseudohypoparathyroidism is maternally inherited and is categorized by hypocalcemia and hyperphosphatemia. Finally, pseudo-pseudohypoparathyroidism is paternally inherited. Patients display normal parathyroid hormone action in the kidney, but exhibit altered parathyroid hormone action in

neg: Ectopic calcification Ectopic calcification Ectopic calcification is a pathologic deposition of calcium salts in tissues or bone growth in soft tissues. This can be a symptom of hyperphosphatemia. Formation of osseous tissue in soft tissues such as the lungs, eyes, arteries, or other organs is known as ectopic calcification, dystrophic calcification, or ectopic ossification. Absorption of calcium salts normally occurs in bony tissues and is facilitated by parathyroid hormone and vitamin D. However, increased amounts of parathyroid hormone in the blood result in the deposit of calcium in soft tissues. This can be an indication of hyperparathyroidism, arteriosclerosis, or trauma to tissues.

neg: Osteopontin and secretion. This is due to the presence of a high-specificity vitamin D response element (VDRE) in the OPN gene promoter. Extracellular inorganic phosphate (ePi) has also been identified as a modulator of OPN expression. Stimulation of OPN expression also occurs upon exposure of cells to pro-inflammatory cytokines, classical mediators of acute inflammation (e.g. tumour necrosis factor α [TNFα], infterleukin-1β [IL-1β]), angiotensin II, transforming growth factor β (TGFβ) and parathyroid hormone (PTH), although a detailed mechanistic understanding of these regulatory pathways are not yet known. Hyperglycemia and hypoxia are also known to increase OPN expression. OPN belongs to a family

neg: 4-Hydroxycoumarins a natural chemical substance of combined plant and fungal origin; mycotoxin also shares these properties. The identification of Dicoumarol in 1940 is the precursor of the drug class known as 4-Hydroxycoumarin. See warfarin for this history. The synthetic drugs in the 4-hydroxycoumarin class are all noted primarily for their use as anticoagulants, though they can have several additional effects. All affect the normal metabolism of vitamin K in the body by inhibiting the enzyme vitamin K epoxide reductase which recycles vitamin K to active form. As such, these compounds form the most important and widely used subset of vitamin K

neg: Pyridoxine 5'-phosphate oxidase and is converted to PLP, the active site of the enzyme is in a partially “closed” conformation. Specific amino acid residues can form hydrogen bonds with the PLP, thus forming a lid that physically covers the active site, giving rise to the “closed” conformation. Pyridoxine 5’-phosphate oxidase is the enzyme that catalyzes the rate-limited step of the B metabolism pathway. Vitamin B, which is also known as pyridoxine, is a crucial nutrient for the human body, as it is responsible for more bodily functions than any other vitamin. Vitamin B is a coenzyme in the metabolism of carbohydrates, fats and

neg: Ernst T. Krebs a vitamin. Pangamic acid, also called "pangamate," and "vitamin B," is the name given to the chemical compound described as d-gluconodimethylamino acetic acid with the empirical formula CHON and purportedly isolated from apricot seeds. It was initially promoted by Ernst T. Krebs, Sr. and his son Ernst T. Krebs, Jr. as a medicinal compound for use in treatment of a wide range of diseases. They also termed this chemical "Vitamin B," though it is not a true vitamin, has no nutritional value, has no known use in the long term treatment of any disease and has been called a "quack

neg: Medication androgens, antiandrogens, estrogens, gonadotropin, corticosteroids, human growth hormone, insulin, antidiabetics (sulfonylureas, biguanides/metformin, thiazolidinediones, insulin), thyroid hormones, antithyroid drugs, calcitonin, diphosponate, vasopressin analogues antifungal, alkalinizing agents, quinolones, antibiotics, cholinergics, anticholinergics, antispasmodics, 5-alpha reductase inhibitor, selective alpha-1 blockers, sildenafils, fertility medications NSAIDs, anticholinergics, haemostatic drugs, antifibrinolytics, Hormone Replacement Therapy (HRT), bone regulators, beta-receptor agonists, follicle stimulating hormone, luteinising hormone, LHRH<br> gamolenic acid, gonadotropin release inhibitor, progestogen, dopamine agonists, oestrogen, prostaglandins, gonadorelin, clomiphene, tamoxifen, Diethylstilbestrol emollients, anti-pruritics, antifungals, disinfectants, scabicides, pediculicides, tar products, vitamin A derivatives, vitamin D analogues, keratolytics, abrasives, systemic antibiotics, topical antibiotics, hormones, desloughing agents, exudate absorbents, fibrinolytics, proteolytics, sunscreens,

neg: Eldecalcitol so as to not hinder bone formation. Unlike other vitamin D analogs, eldecalcitol does not significantly suppress parathyroid hormone levels, promising a better treatment for osteoporosis in comparison to other medications. Bone mineral density increases with eldecalcitol use, in addition to strengthening bone structure. This occurs due to the function of the eldecalcitol drug, which decreases bone reabsorption as observed through a bone reabsorption marker. Bone geometry assessments show that eldecalcitol increases cortical bone area in patients with osteoporosis more so than other vitamin D analogs, such as alfacalcidol. There was also the maintenance of thickness of cortical bone mass,

neg: Steroid hormone Steroid hormone A steroid hormone is a steroid that acts as a hormone. Steroid hormones can be grouped into two classes: corticosteroids (typically made in the adrenal cortex, hence "cortico-") and sex steroids (typically made in the gonads or placenta). Within those two classes are five types according to the receptors to which they bind: glucocorticoids, mineralocorticoids (corticosteroids), androgens, estrogens, and progestogens (sex steroids). Vitamin D derivatives are a sixth closely related hormone system with homologous receptors. They have some of the characteristics of true steroids as receptor ligands. Steroid hormones help control metabolism, inflammation, immune functions, salt and water

neg: Immunostimulant Immunostimulant Immunostimulants, also known as immunostimulators, are substances (drugs and nutrients) that stimulate the immune system by inducing activation or increasing activity of any of its components. One notable example is the granulocyte macrophage colony-stimulating factor. There are two main categories of immunostimulants: Many endogenous substances are non-specific immunostimulators. For example, female sex hormones are known to stimulate both adaptive and innate immune responses. Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty. Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D. Some

neg: Vitamin growth and differentiation. The B complex vitamins function as enzyme cofactors (coenzymes) or the precursors for them. Vitamin D has a hormone-like function as a regulator of mineral metabolism for bones and other organs. Vitamins C and E function as antioxidants. Both deficient and excess intake of a vitamin can potentially cause clinically significant illness; although excess intake of water-soluble vitamins is less likely to do so. Before 1935, the only source of vitamins was from food. If intake of vitamins was lacking, the result was vitamin deficiency and consequent deficiency diseases. Then, commercially produced tablets of yeast-extract vitamin B

neg: Rickets to a maternal shortage of vitamin D; and people with darker skins need more sunlight to maintain vitamin D levels. Rickets had historically been a problem in London, especially during the Industrial Revolution. Persistent thick fog and heavy industrial smog permeating the city blocked out significant amounts of sunlight to such an extent that up to 80 percent of children at one time had varying degrees of rickets in one form or the other. It is sometimes known in German as "the English Disease" (Die englische Krankheit) Vitamin D natural selection hypotheses: Rickets is often a result of vitamin D3