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Which Of The Following Is The Animal Form Of Vitamin K, Produced By Bacteria In The Large Intestine?

Structurally similar, fatty-soluble vitamers plant in foods and marketed as dietary supplements

Vitamin K
Drug class
K-Vitamine.svg

Vitamin K structures.

Class identifiers
Use Vitamin M deficiency, Warfarin overdose
ATC code B02BA
Biological target Gamma-glutamyl carboxylase
Clinical data
Drugs.com Medical Encyclopedia
External links
MeSH D014812
In Wikidata

Vitamin Grand refers to structurally like, fat-soluble vitamers plant in foods and marketed as dietary supplements.[1] The human body requires vitamin K for mail service-synthesis modification of certain proteins that are required for blood coagulation (Grand from koagulation, German for "coagulation") or for controlling binding of calcium in bones and other tissues.[two] The complete synthesis involves final modification of these so-called "Gla proteins" past the enzyme gamma-glutamyl carboxylase that uses vitamin K as a cofactor.

Vitamin K is used in the liver every bit the intermediate VKH2 to deprotonate a glutamate residue then is reprocessed into vitamin Chiliad through a vitamin Yard oxide intermediate.[3] The presence of uncarboxylated proteins indicates a vitamin Thousand deficiency. Carboxylation allows them to bind (chelate) calcium ions, which they cannot do otherwise.[4] Without vitamin K, blood coagulation is seriously impaired, and uncontrolled bleeding occurs. Research suggests that deficiency of vitamin K may also weaken bones, potentially contributing to osteoporosis, and may promote calcification of arteries and other soft tissues.[2] [iv] [5]

Chemically, the vitamin Thou family unit comprises 2-methyl-1,four-naphthoquinone (3-) derivatives. Vitamin M includes two natural vitamers: vitamin Ki (phylloquinone) and vitamin One thousandtwo (menaquinone).[four] Vitamin K2, in turn, consists of a number of related chemical subtypes, with differing lengths of carbon side chains made of isoprenoid groups of atoms. The two well-nigh studied ones are menaquinone-iv (MK-iv) and menaquinone-7 (MK-seven).

Vitamin One thousand1 is made by plants, and is found in highest amounts in green leafy vegetables, because it is straight involved in photosynthesis. It is active as a vitamin in animals and performs the classic functions of vitamin K, including its action in the production of blood-clotting proteins. Animals may also convert information technology to vitamin K2, variant MK-four. Bacteria in the gut flora can also convert Thousand1 into MK-4. All forms of 1000ii other than MK-4 can only be produced past leaner, which utilize these during anaerobic respiration. Vitamin K3 (menadione), a synthetic form of vitamin K, was used to treat vitamin K deficiency, but because it interferes with the function of glutathione, it is no longer used this way in human nutrition.[2]

Definition [edit]

Vitamin K refers to structurally similar, fat-soluble vitamers found in foods and marketed equally dietary supplements. "Vitamin Yard" include several chemical compounds. These are similar in construction in that they share a quinone ring, but differ in the length and degree of saturation of the carbon tail and the number of repeating isoprene units in the side chain (see figures in Chemistry section). Plant-sourced forms are primarily vitamin K1. Animal-sourced foods are primarily vitamin K2.[i] [6] [7] Vitamin K has several roles: an essential nutrient captivated from food, a product synthesized and marketed as part of a multi-vitamin or as a single-vitamin dietary supplement, and a prescription medication for specific purposes.[1]

Dietary recommendations [edit]

The U.s. National University of Medicine does not distinguish betwixt Kane and Kii – both are counted as vitamin K. When recommendations were last updated in 1998, sufficient data was not available to establish an estimated boilerplate requirement or recommended dietary allowance, terms that be for most vitamins. In instances such equally these, the academy defines acceptable intakes (AIs) as amounts that appear to be sufficient to maintain good wellness, with the agreement that at some later date, AIs volition be replaced by more than verbal data. The electric current AIs for developed women and men ages 19 and older are ninety and 120 ÎŒg/day, respectively, for pregnancy is 90 ÎŒg/day, and for lactation is xc ÎŒg/day. For infants upwards to 12 months, the AI is 2.0–2.5 ÎŒg/day; for children ages 1–18 years the AI increases with age from 30 to 75 ÎŒg/day. As for rubber, the academy sets tolerable upper intake levels (known every bit "upper limits") for vitamins and minerals when evidence is sufficient. Vitamin Yard has no upper limit, equally human data for agin effects from high doses are not sufficient.[5]

In the Eu, adequate intake is divers the same style as in the U.s.. For women and men over age xviii the adequate intake is set at seventy ÎŒg/day, for pregnancy lxx ÎŒg/day, and for lactation 70 ÎŒg/day. For children ages i–17 years, adequate intake values increment with age from 12 to 65 ÎŒg/twenty-four hours.[eight] Nippon set adequate intakes for adult women at 65 ÎŒg/mean solar day and for men at 75 ÎŒg/day.[9] The European union and Nihon also reviewed safety and concluded – every bit had the U.s.a. – that there was insufficient prove to set an upper limit for vitamin K.[ix] [x]

For The states nutrient and dietary supplement labeling purposes, the corporeality in a serving is expressed as a percentage of daily value. For vitamin K labeling purposes, 100% of the daily value was 80 ÎŒg, but on 27 May 2016 it was revised upwards to 120 ÎŒg, to bring it into agreement with the highest value for adequate intake.[eleven] [12] Compliance with the updated labeling regulations was required by ane January 2020 for manufacturers with US$x million or more in almanac nutrient sales, and by 1 January 2021 for manufacturers with lower volume food sales.[13] [14] A table of the old and new developed daily values is provided at Reference Daily Intake.

Fortification [edit]

According to the Global Fortification Data Exchange, vitamin Chiliad deficiency is so rare that no countries crave that foods be fortified.[15] The Globe Wellness Organization does non have recommendations on vitamin Thousand fortification.[xvi]

Sources [edit]

Vitamin M1 is primarily from plants, especially leafy light-green vegetables. Small-scale amounts are provided by beast-sourced foods. Vitamin K2 is primarily from animal-sourced foods, with poultry and eggs much better sources than beef, pork or fish.[7] One exception to the latter is nattƍ, which is made from bacteria-fermented soybeans. It is a rich food source of vitamin K2 variant MK-7, made by the bacteria.[17]

Vitamin One thousand1 [edit]

Establish-sourced[seven] Amount Chiliad1
(ÎŒg / measure)
Collard greens boiled, drained, 1two cup 530
Spinach boiled, drained, i2 cup 445
Turnip greens boiled, drained, 12 loving cup 425
Spinach raw, one cup 145
Brussels sprouts boiled, drained, anetwo cup 110
Kale raw, i cup 82
Broccoli boiled, tuckered, one2 loving cup 81
Asparagus boiled, tuckered, 4 spears 48
Kiwifruit peeled, sliced, 12 cup 36
Chinese cabbage cooked, 1two cup 29
Blueberries frozen, 12 cup 21
Carrots raw, chopped, 1 cup 17
Plant-sourced[7] Amount K1
(ÎŒg / mensurate)
Hazelnuts chopped, ane cup 16
Grapes, 12 cup 11
Tomato products, 1 cup 9.ii
Olive oil, 1.0 tablespoon viii.one
Zucchini boiled, drained, 1.0 loving cup vii.6
Mangos pieces, one.0 cup 6.9
Pears, pieces, 1.0 loving cup vi.two
Irish potato broiled, including skin, one half-dozen.0
Sweet murphy baked, one ii.six
Bread whole wheat, i slice 2.5
Bread white, 1 piece 2.2
Animal-sourced[7] Corporeality Ki
(ÎŒg / mensurate)
Craven, 4.0 oz 2.7–3.3
Mollusks, 4 oz 2.two
Cheese diced, 1two cup 1.4–1.7
Beefiness, 4 oz 0.9
Pork sausage, 4 oz 0.9
Yogurt whole milk, ane.0 cup 0.4
Milk whole or low fat, 1.0 cup 0.2
Fish, 4 oz 0.1
Eggs, one 0.1
Human milk, per liter 0.85–9.ii (median ii.5)[18]

Vitamin Ktwo [edit]

Brute-sourced foods are a source of vitamin K2 [nineteen] [20] The MK-4 form is from conversion of plant-sourced vitamin Kane in various tissues in the body.[21]

Vitamin deficiency [edit]

Because vitamin One thousand aids mechanisms for blood clotting, its deficiency may lead to reduced blood clotting, and in severe cases, tin can result in reduced clotting, increased bleeding, and increased prothrombin fourth dimension.[ii] [five]

Normal diets are unremarkably not deficient in vitamin K, indicating that deficiency is uncommon in healthy children and adults.[iv] An exception may be infants who are at an increased run a risk of deficiency regardless of the vitamin status of the mother during pregnancy and breast feeding due to poor transfer of the vitamin to the placenta and low amounts of the vitamin in chest milk.[xviii]

Secondary deficiencies tin can occur in people who consume adequate amounts, merely have malabsorption weather condition, such as cystic fibrosis or chronic pancreatitis, and in people who have liver damage or disease.[2] Secondary vitamin K deficiency tin can besides occur in people who have a prescription for a vitamin One thousand antagonist drug, such as warfarin.[ii] [4] A drug associated with increased risk of vitamin K deficiency is cefamandole, although the mechanism is unknown.[22]

Medical uses [edit]

Treating vitamin deficiency in newborns [edit]

Vitamin K is given every bit an injection to newborns to prevent vitamin K deficiency bleeding.[18] The blood clotting factors of newborn babies are roughly xxx–threescore% that of adult values; this appears to be a consequence of poor transfer of the vitamin across the placenta, and thus depression fetal plasma vitamin K.[18] Occurrence of vitamin K deficiency haemorrhage in the first week of the infant's life is estimated at 0.25–1.7%, with a prevalence of 2–10 cases per 100,000 births. Human milk contains 0.85–nine.two ÎŒg/L (median ii.v ÎŒg/L) of vitamin Ki, while infant formula is formulated in range of 24–175 ÎŒg/50.[xviii] Tardily onset bleeding, with onset 2 to 12 weeks after birth, can be a outcome of exclusive breastfeeding, especially if there was no preventive treatment.[18] Late onset prevalence reported at 35 cases per 100,000 live births in infants who had not received prophylaxis at or shortly after birth.[23] Vitamin Chiliad deficiency haemorrhage occurs more than oft in the Asian population compared to the Caucasian population.[18]

Haemorrhage in infants due to vitamin K deficiency can be severe, leading to hospitalization, brain impairment, and death. Intramuscular injection, typically given shortly after nascence, is more effective in preventing vitamin K deficiency haemorrhage than oral administration, which calls for weekly dosing up to 3 months of age.[18]

Managing warfarin therapy [edit]

Warfarin is an anticoagulant drug. Information technology functions by inhibiting an enzyme that is responsible for recycling vitamin K to a functional land. As a consequence, proteins that should be modified by vitamin Thou are not, including proteins essential to blood clotting, and are thus not functional.[24] The purpose of the drug is to reduce risk of inappropriate blood clotting, which can have serious, potentially fatal consequences.[2] The proper anticoagulant action of warfarin is a function of vitamin Grand intake and drug dose. Due to differing absorption of the drug and amounts of vitamin Grand in the diet, dosing must be monitored and individualized for each patient.[25] Some foods are so high in vitamin Kone that medical advice is to avert those (examples: collard greens, spinach, turnip greens) entirely, and for foods with a modestly high vitamin content, keep consumption as consequent as possible, and then that the combination of vitamin intake and warfarin keep the anti-clotting action in the therapeutic range.[26]

Vitamin K is a treatment for bleeding events caused by overdose of the drug.[27] The vitamin can be administered by oral cavity, intravenously or subcutaneously.[27] Oral vitamin Thousand is used in situations when a person'due south International normalised ratio is greater than 10 but there is no agile bleeding.[26] [28] The newer anticoagulants apixaban, dabigatran and rivaroxaban are not vitamin K antagonists.[29]

Treating rodenticide poisoning [edit]

Coumarin is used in the pharmaceutical manufacture as a precursor reagent in the synthesis of a number of constructed anticoagulant pharmaceuticals.[30] One subset, iv-hydroxycoumarins, act as vitamin Grand antagonists. They block the regeneration and recycling of vitamin Thou. Some of the 4-hydroxycoumarin anticoagulant class of chemicals are designed to have high potency and long residence times in the trunk, and these are used specifically as 2d generation rodenticides ("rat toxicant"). Decease occurs afterwards a period of several days to ii weeks, usually from internal hemorrhaging.[30] For humans, and for animals that take consumed either the rodenticide or rats poisoned past the rodenticide, treatment is prolonged administration of large amounts of vitamin Yard.[31] [32] This dosing must sometimes exist continued for up to 9 months in cases of poisoning by "superwarfarin" rodenticides such as brodifacoum. Oral vitamin One thousandone is preferred over other vitamin Yard1 routes of administration because it has fewer side effects.[33]

Methods of assessment [edit]

An increase in prothrombin fourth dimension, a coagulation assay, has been used as an indicator of vitamin Thousand status, but it lacks sufficient sensitivity and specificity for this application.[34] Serum phylloquinone is the well-nigh commonly used marker of vitamin K status. Concentrations <0.15 Â”g/50 are indicative of deficiency. Disadvantages include exclusion of the other vitamin K vitamers and interference from recent dietary intake.[34] Vitamin K is required for the gamma-carboxylation of specific glutamic acrid residues within the Gla domain of the 17 vitamin Yard–dependent proteins. Thus, a rise in uncarboxylated versions of these proteins is an indirect but sensitive and specific marker for vitamin K deficiency. If uncarboxylated prothrombin is being measured, this "Protein induced by Vitamin Grand Absence/antagonism (PIVKA-Ii)" is elevated in vitamin G deficiency. The test is used to assess risk of vitamin M–scarce bleeding in newborn infants.[34] Osteocalcin is involved in calcification of bone tissue. The ratio of uncarboxylated osteocalcin to carboxylated osteocalcin increases with vitamin Chiliad deficiency. Vitamin K2 has been shown to lower this ratio and improve lumbar vertebrae bone mineral density.[35] Matrix Gla protein must undergo vitamin K dependent phosphorylation and carboxylation. Elevated plasma concentration of dephosphorylated, uncarboxylated MGP is indicative of vitamin K deficiency.[36]

Side effects [edit]

No known toxicity is associated with loftier oral doses of the vitamin One thousand1 or (vitamin K2) forms of vitamin K, so regulatory agencies from US, Japan and European Marriage hold that no tolerable upper intake levels needs to be set.[5] [9] [10] However, vitamin Grand1 has been associated with severe adverse reactions such equally bronchospasm and cardiac arrest when given intravenously. The reaction is described as a nonimmune-mediated anaphylactoid reaction, with incidence of iii per 10,000 treatments. The majority of reactions occurred when polyoxyethylated brush oil was used as the solubilizing amanuensis.[37]

Not-human uses [edit]

Forms non establish in nature, and thus not "vitamins", are menadione and 4-amino-ii-methyl-one-naphthol ("Chiliad5"). Menadione, a synthetic compound sometimes referred to equally vitamin Giii, is used in the pet food industry because once consumed it is converted to vitamin K2.[38] The US Food and Drug Administration has banned this form from sale as a human dietary supplement because big doses have been shown to cause allergic reactions, hemolytic anemia, and cytotoxicity in liver cells.[2] Research with Yard5 suggests it may inhibit fungal growth in fruit juices.[39]

Chemistry [edit]

Vitamin Kone (phylloquinone) – both forms of the vitamin incorporate a functional naphthoquinone ring and an aliphatic side concatenation. Phylloquinone has a phytyl side concatenation.

Vitamin Thousandii (menaquinone). In menaquinone, the side chain is composed of a varying number of isoprenoid residues. The most common number of these residues is four, since animal enzymes normally produce menaquinone-four from establish phylloquinone.

The structure of phylloquinone, Vitamin Yard1, is marked past the presence of a phytyl sidechain.[5] Vitamin Grandone has an (Eastward) trans double bond responsible for its biological activeness, and two chiral centers on the phytyl sidechain.[40] Vitamin Chiliadone appears as a yellow viscous liquid at room temperature due to its absorption of violet light in the UV-Vis Spectra.[41] The structures of menaquinones, vitamin K2, are marked by the polyisoprenyl side chain present in the molecule that can contain 4 to 13 isoprenyl units. MK-four is the most common form. [five] The big size of Vitamin K1 gives many different peaks in mass spectroscopy, most of which involve derivatives of the naphthoquinone ring base and the alkyl side chain.[42]

A sample of phytomenadione for injection, as well called phylloquinone

Conversion of vitamin K1 to vitamin Ktwo [edit]

In animals, the MK-four form of vitamin K2 is produced by conversion of vitamin K1 in the testes, pancreas, and arterial walls.[21] While major questions all the same surround the biochemical pathway for this transformation, the conversion is not dependent on gut leaner, as it occurs in germ-costless rats[43] and in parenterally administered K1 in rats.[44] [45] At that place is testify that the conversion proceeds past removal of the phytyl tail of One thousand1 to produce menadione (also referred to equally vitamin One thousand3) as an intermediate, which is and then prenylated to produce MK-4.[46]

Physiology [edit]

In animals, vitamin One thousand is involved in the carboxylation of certain glutamate residues in proteins to class gamma-carboxyglutamate (Gla) residues. The modified residues are often (but not ever) situated within specific protein domains called Gla domains. Gla residues are usually involved in binding calcium, and are essential for the biological activity of all known Gla proteins.[47]

17 human proteins with Gla domains have been discovered; they play key roles in the regulation of three physiological processes:

  • Claret coagulation: prothrombin (factor Ii), factors 7, IX, and Ten, and proteins C, S, and Z[48]
  • Bone metabolism: osteocalcin, matrix Gla protein (MGP),[49] periostin,[50] and Gla-rich protein.[51] [52]
  • Vascular biology: Matrix Gla protein, growth arrest – specific poly peptide half dozen (Gas6)[53]
  • Unknown functions: proline-rich Îł-carboxyglutamyl proteins ane and 2, and transmembrane Îł-carboxy glutamyl proteins 3 and 4.[54]

Absorption [edit]

Vitamin K is absorbed through the jejunum and ileum in the small intestine. The process requires bile and pancreatic juices. Estimates for absorption are on the order of fourscore% for vitamin Kane in its costless course (as a dietary supplement) just much lower when nowadays in foods. For case, the absorption of vitamin Grand from kale and spinach – foods identified as having a loftier vitamin K content – are on the social club of 4% to 17% regardless of whether raw or cooked.[4] Less information is available for absorption of vitamin Yardii from foods.[four] [5]

The intestinal membrane protein Niemann–Choice C1-similar 1 (NPC1L1) mediates cholesterol absorption. Beast studies show that information technology also factors into absorption of vitamins East and K1.[55] The same study predicts potential interaction betwixt SR-BI and CD36 proteins every bit well.[55] The drug ezetimibe inhibits NPC1L1 causing a reduction in cholesterol absorption in humans, and in fauna studies, also reduces vitamin Due east and vitamin K1 assimilation. An expected consequence would be that administration of ezetimibe to people who take warfarin (a vitamin K antagonist) would potentiate the warfarin issue. This has been confirmed in humans.[55]

Biochemistry [edit]

Office in animals [edit]

Cyclic mechanism of action of vitamin M

In both cases R represents the isoprenoid side chain.

Vitamin One thousand is distributed differently inside animals depending on its specific homologue. Vitamin K1 is mainly present in the liver, center and pancreas, while MK-4 is ameliorate represented in the kidneys, brain and pancreas. The liver too contains longer chain homologues MK-7 to MK-thirteen.[56]

The role of vitamin K2 in the animate being cell is to add a carboxylic acid functional grouping to a glutamate (Glu) amino acid residue in a protein, to form a gamma-carboxyglutamate (Gla) remainder. This is a somewhat uncommon posttranslational modification of the poly peptide, which is and then known every bit a "Gla protein". The presence of two −COOH (carboxylic acrid) groups on the same carbon in the gamma-carboxyglutamate remainder allows it to chelate calcium ions. The binding of calcium ions in this way very often triggers the function or bounden of Gla-protein enzymes, such as the so-called vitamin 1000–dependent clotting factors discussed beneath.[57]

Within the cell, vitamin K participates in a cyclic process. The vitamin undergoes electron reduction to a reduced form called vitamin G hydroquinone, catalyzed by the enzyme vitamin K epoxide reductase (VKOR).[58] Another enzyme then oxidizes vitamin K hydroquinone to allow carboxylation of Glu to Gla; this enzyme is called gamma-glutamyl carboxylase[59] or the vitamin K–dependent carboxylase. The carboxylation reaction just gain if the carboxylase enzyme is able to oxidize vitamin One thousand hydroquinone to vitamin K epoxide at the same time. The carboxylation and epoxidation reactions are said to be coupled. Vitamin K epoxide is so restored to vitamin One thousand past VKOR. The reduction and subsequent reoxidation of vitamin G coupled with carboxylation of Glu is called the vitamin K bicycle.[lx] Humans are rarely deficient in vitamin Yard considering, in function, vitamin Chiliad2 is continuously recycled in cells.[61]

Warfarin and other 4-hydroxycoumarins cake the action of VKOR.[24] This results in decreased concentrations of vitamin Grand and vitamin G hydroquinone in tissues, such that the carboxylation reaction catalyzed by the glutamyl carboxylase is inefficient. This results in the production of clotting factors with inadequate Gla. Without Gla on the amino termini of these factors, they no longer demark stably to the blood vessel endothelium and cannot activate clotting to allow germination of a jell during tissue injury. As information technology is impossible to predict what dose of warfarin will give the desired caste of clotting suppression, warfarin treatment must be carefully monitored to avert underdose and overdose.[25]

Gamma-carboxyglutamate proteins [edit]

The following human Gla-containing proteins ("Gla proteins") have been characterized to the level of primary structure: blood coagulation factors Two (prothrombin), VII, 9, and X, anticoagulant protein C and protein South, and the gene X-targeting poly peptide Z. The bone Gla protein osteocalcin, the calcification-inhibiting matrix Gla protein (MGP), the cell growth regulating growth arrest specific gene 6 protein, and the 4 transmembrane Gla proteins, the part of which is at present unknown. The Gla domain is responsible for high-affinity binding of calcium ions (Ca2+) to Gla proteins, which is often necessary for their conformation, and always necessary for their function.[57]

Gla proteins are known to occur in a wide diversity of vertebrates: mammals, birds, reptiles, and fish. The venom of a number of Australian snakes acts past activating the human being blood-clotting system. In some cases, activation is achieved by snake Gla-containing enzymes that demark to the endothelium of human blood vessels and catalyze the conversion of procoagulant clotting factors into activated ones, leading to unwanted and potentially mortiferous clotting.[62]

Some other interesting class of invertebrate Gla-containing proteins is synthesized by the fish-hunting snail Conus geographus.[63] These snails produce a venom containing hundreds of neuroactive peptides, or conotoxins, which is sufficiently toxic to kill an adult human. Several of the conotoxins incorporate two to five Gla residues.[64]

Function in plants [edit]

Vitamin Chiliadi is an important chemical in dark-green plants, where it functions as an electron acceptor in photosystem I during photosynthesis.[65] For this reason, vitamin K1 is found in large quantities in the photosynthetic tissues of plants (green leaves, and night green leafy vegetables such every bit romaine lettuce, kale, and spinach), but it occurs in far smaller quantities in other plant tissues.[7] [65]

Role in bacteria [edit]

Many bacteria, including Escherichia coli found in the large intestine, can synthesize vitamin Ktwo (MK-7 up to MK-xi),[66] but non vitamin G1. Dark-green algae and some species of cyanobacteria (sometimes referred to every bit blue-light-green algae) are able to synthesize vitamin Kone.[65] In the vitamin K2 synthesizing leaner, menaquinone transfers two electrons between two different small molecules, during oxygen-contained metabolic energy product processes (anaerobic respiration).[67] For instance, a pocket-size molecule with an excess of electrons (too chosen an electron donor) such equally lactate, formate, or NADH, with the help of an enzyme, passes two electrons to menaquinone. The menaquinone, with the aid of another enzyme, and so transfers these two electrons to a suitable oxidant, such as fumarate or nitrate (also called an electron acceptor). Adding 2 electrons to fumarate or nitrate converts the molecule to succinate or nitrite plus water, respectively.[67] Some of these reactions generate a cellular free energy source, ATP, in a mode similar to eukaryotic jail cell aerobic respiration, except the final electron acceptor is not molecular oxygen, merely fumarate or nitrate. In aerobic respiration, the final oxidant is molecular oxygen, which accepts iv electrons from an electron donor such equally NADH to be converted to h2o. E. coli, equally facultative anaerobes, tin comport out both aerobic respiration and menaquinone-mediated anaerobic respiration.[67]

History [edit]

In 1929, Danish scientist Henrik Dam investigated the role of cholesterol past feeding chickens a cholesterol-depleted diet.[68] He initially replicated experiments reported by scientists at the Ontario Agronomical College.[69] McFarlane, Graham and Richardson, working on the chick feed programme at OAC, had used chloroform to remove all fat from chick grub. They noticed that chicks fed only fatty-depleted chow developed hemorrhages and started bleeding from tag sites.[70] Dam found that these defects could non be restored by adding purified cholesterol to the diet. It appeared that – together with the cholesterol – a 2d compound had been extracted from the food, and this compound was called the coagulation vitamin. The new vitamin received the letter K because the initial discoveries were reported in a German journal, in which it was designated as Koagulationsvitamin. Edward Adelbert Doisy of Saint Louis Academy did much of the research that led to the discovery of the construction and chemical nature of vitamin K.[71] Dam and Doisy shared the 1943 Nobel Prize for medicine for their work on vitamin Grand1 and Thoutwo published in 1939. Several laboratories synthesized the compound(south) in 1939.[72]

For several decades, the vitamin Grand–deficient chick model was the only method of quantifying vitamin K in various foods: the chicks were made vitamin Yard–scarce and subsequently fed with known amounts of vitamin K–containing nutrient. The extent to which blood coagulation was restored by the diet was taken equally a measure for its vitamin K content. Three groups of physicians independently establish this: Biochemical Establish, University of Copenhagen (Dam and Johannes Glavind), University of Iowa Department of Pathology (Emory Warner, Kenneth Brinkhous, and Harry Pratt Smith), and the Mayo Clinic (Hugh Butt, Albert Snell, and Arnold Osterberg).[73]

The first published report of successful treatment with vitamin K of life-threatening hemorrhage in a jaundiced patient with prothrombin deficiency was made in 1938 by Smith, Warner, and Brinkhous.[74]

The precise role of vitamin Yard was not discovered until 1974, when prothrombin, a claret coagulation protein, was confirmed to be vitamin Thousand dependent. When the vitamin is present, prothrombin has amino acids nigh the amino terminus of the protein as Îł-carboxyglutamate instead of glutamate, and is able to bind calcium, part of the clotting procedure.[75]

Research [edit]

Osteoporosis [edit]

Vitamin K is required for the gamma-carboxylation of osteocalcin in os.[76] The take a chance of osteoporosis, assessed via bone mineral density and fractures, was not affected for people on warfarin therapy – a vitamin Grand antagonist.[77] College dietary intake of vitamin Chiliadone may modestly decrease the run a risk of fractures.[78] However, in that location is mixed evidence to support a claim that vitamin K supplementation reduces hazard of bone fractures.[iv] [76] [79] For women who were mail service-menopausal and for all people diagnosed with osteoporosis, supplementation trials reported increases in bone mineral density, a reduction to the odds of any clinical fractures but no meaning departure for vertebral fractures.[79] There is a subset of literature on supplementation with vitamin Ktwo MK-four and bone health. A meta-analysis reported a decrease in the ratio of uncarboxylated osteocalcin to carboxylated, an increase in lumbar spine bone mineral density, but no significant differences for vertebral fractures.[35]

Cardiovascular health [edit]

Matrix Gla protein is a vitamin K-dependent protein plant in bone, merely likewise in soft tissues such equally arteries, where information technology appears to function as an anti-calcification poly peptide. In animal studies, animals that lack the gene for MGP exhibit calcification of arteries and other soft tissues.[iv] In humans, Keutel syndrome is a rare recessive genetic disorder associated with abnormalities in the gene coding for MGP and characterized by abnormal lengthened cartilage calcification.[80] These observations led to a theory that in humans, inadequately carboxylated MGP, due to low dietary intake of the vitamin, could result in increased risk of arterial calcification and coronary middle disease.[4]

In meta-analyses of population studies, depression intake of vitamin K was associated with inactive MGP, arterial calcification[81] and arterial stiffness.[82] [83] Lower dietary intakes of vitamin Chiliad1 and vitamin Thou2 were as well associated with higher coronary heart disease.[36] [84] When claret concentration of circulating vitamin 10001 was assessed in that location was an increased risk in all cause mortality linked to low concentration.[85] [86] In contrast to these population studies, a review of randomized trials using supplementation with either vitamin One thousand1 or vitamin K2 reported no part in mitigating vascular calcification or reducing arterial stiffness. The trials were too short to assess whatsoever impact on coronary center disease or mortality.[87]

Other [edit]

Population studies propose that vitamin K status may accept roles in inflammation, brain office, endocrine part and an anti-cancer effect. For all of these, there is non sufficient evidence from intervention trials to draw any conclusions.[4] From a review of observational trials, long-term utilize of vitamin Chiliad antagonists as anticoagulation therapy is associated with lower cancer incidence in general.[88] In that location are alien reviews as to whether agonists reduce the run a risk of prostate cancer.[89] [xc]

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Further reading [edit]

  • "Vitamin Thou: Some other Reason to Eat Your Greens" (PDF). Agricultural Research. 48 (1). January 2000. ISSN 2169-8244.

External links [edit]

  • "Vitamin Thou". Drug Information Portal. U.S. National Library of Medicine.
  • "Phylloquinone". Drug Information Portal. U.S. National Library of Medicine.
  • "Phytomenadione". Drug Information Portal. U.S. National Library of Medicine.
  • "Vitamin K2". Drug Data Portal. U.S. National Library of Medicine.
  • "Menadione". Drug Information Portal. U.South. National Library of Medicine.

Source: https://en.wikipedia.org/wiki/Vitamin_K

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