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Las '''menaquinonas''' o '''vitaminas {{fquim|K|2}}''', es el nombre de grupo dado a una familia de compuestos relacionados, generalmente divididos en menaquinonas de cadena corta (de la cual la [[menatetrenona]] o MK-4, es el miembro más importante), y las menaquinonas de cadena larga, de las cuales MK-7, MK-8 y MK-9 son las más reconocidas desde el punto de vista nutricional. |
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#REDIRECCIÓN [[Vitamina K]] |
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== Formas == |
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[[File:Vitamin K structures.jpg|thumb|right|300px|Estructuras de vitaminas K. Las MK-4 y MK-7 son ambas subtipos de {{fquim|K|2}}.]] |
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{{AP|Vitamina K}} |
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Todas las vitaminas K son similares en estructura; comparten un núcleo formado por un anillo [[quinona]], pero difieren en la longitud y grado de saturación de la cola carbonada y del número de cadenas laterales que esta posee.<ref>Shearer MJ.2003 in Physiology. Elsevier Sciences LTD. 6039-45.</ref> El número de cadenas laterales se encuentra indicado en el nombre particular de cada menaquinona (por ejemplo, MK-4 significa que cuatro unidades moleculares de tipo [[isopreno]] se encuentran unidas a la cola carbonada), y esto influencia el transporte a diferentes tejidos diana. |
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== Mecanismo de acción == |
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El [[mecanismo de acción]] de la vitamina {{fquim|K|2}} es similar al de la vitamina {{fquim|K|1}}. Tradicionalmente, las vitaminas K son reconocidas como un factor requerido para la coagulación, pero las funciones desempeñadas por este grupo de vitaminas se revela mucho más complejo. Las vitaminas K desempeñan un papel esencial como cofactor de la enzima [[gama-glutamil carboxilasa]], la cual se encuentra involucrada en la carboxilación de las proteínas dependientes de vitamina K, esto es la conversión de los ácidos glutámicos (Glu) que forman parte de un péptido, a ácido γ-carboxi glutámico (Gla). |
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[[File:Carboxylation reaction vitamin K cycle.png|thumb|center|500px|Reacción de carboxilación, ''ciclo de la vitamina K'']]. |
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La [[carboxilación]] de proteínas dependientes de vitamina K, conocidas como [[Dominio Gla|Proteínas Gla]], es un proceso importante y sirve como vía de reciclaje para recuperar a la vitamina K de sus metabolitos de tipo [[epóxido]] (K0) para su reutilización en carboxilaciones. Se han descubierto varias proteínas humanas que contienen el dominio Gla y que son sintetizadas en diferentes tipos de tejidos: |
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* [[Factor de coagulación|Factores de la coagulación]] (II, VII, IX, X), como así también las proteínas anticoagulantes (C, S, Z). Estas proteínas Gla se sintetizan en el [[hígado]] y desempeñan un importante papel en la homeostasis sanguínea. |
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* [[Osteocalcina]]. Esta proteína no colágena es secretada por los [[osteoblastos]] y desempeña un papel primordial en la mineralización del hueso. |
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* [[Proteína Gla matriz]] (MGP). Esta proteína inhibidora de la calcificación, se encuentra en numerosos tejidos, pero su papel más importante lo desempeña en [[cartílago]] y paredes de vasos arteriales. |
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* [[GAS6|Proteína específica de detención del crecimiento 6]] (GAS6). La GAS6 se secreta en los linfocitos y células endoteliales en respuesta al daño y ayuda a la supervivencia celular, proliferación, migración y adhesión. |
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* Proteínas Gla ricas en prolina (PRGP), proteínas Gla transmembrana (TMG) y periostina (GRP), cuya función precisa aún no ha sido explorada. |
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==Health effects== |
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===Bone density=== |
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It has been suggested that vitamin K<sub>2</sub> may play an important role in maintaining healthy levels of [[bone mineral density]] (BMD). However, data on the subject is inconclusive - some clinical trials show no improvement of BMD after vitamin K supplementation. First indications came from patients with femoral neck fractures, who demonstrated an extremely low level of circulating vitamin K<sub>2</sub>. The strong association between vitamin K<sub>2</sub> deficiency and impaired bone health was later proved by both laboratory and clinical studies. It has been found that vitamin K<sub>2</sub> deficiency results in a decreased level of active osteocalcin, which in turn increases the risk for fragile bones.<ref>Booth et al. (July 2, 2013) "Associations between Vitamin K Biochemical Measures and Bone Mineral Density in Men and Women", ''The Journal of Clinical Endocrinology & Metabolism'' Vol.89 No.10 pp.4904-9 {{doi|10.1210/jc.2003-031673}}</ref><ref>Knapen MH, Nieuwenhuijzen Kruseman AC, Wouters RS, Vermeer C. (Nov 1998) "Correlation of serum osteocalcin fractions with bone mineral density in women during the first 10 years after menopause", ''Calcified Tissue International'' Vol.63 No.5 pp.375-9, [[International Osteoporosis Foundation]] {{doi|10.1007/s002239900543}}</ref> Research also showed that vitamin K<sub>2</sub>, but not K<sub>1</sub> in combination with calcium and vitamin D can decrease bone turnover.<ref>[http://www.sciencedirect.com/science/article/pii/S0531513106005437 Schurgers LJ,Knapen MH, Vermeer C. Vitamin (March 2007) "K<sub>2</sub> supplementation improves hip bone geometry and bone strength indices in postmenopausal women",] ''International Congress Series'' Vol. 1297 pp. 179-187, Nutritional Aspects of Osteoporosis 2006. Proceedings of the 6th International Symposium on Nutritional Aspects of Osteoporosis, 4–6 May 2006, Lausanne, Switzerland</ref> Moreover, a study performed by Knapen et al. clearly demonstrated that vitamin K<sub>2</sub> is essential for the maintenance of bone strength in postmenopausal women, and was the factor for improving bone mineral content and femoral neck width.<ref>Knapen MH, Schurgers LJ, Vermeer C. (July 2007) "Vitamin K<sub>2</sub> supplementation improves hip bone geometry and bone strength indices in postmenopausal women", ''Osteoporosis International'' Vol.18 No.7 pp.963-72 {{doi| 10.1007/s00198-007-0337-9}}</ref> |
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More arguments supporting the unique function of vitamin K<sub>2</sub> came from Japan. The Japanese population seems to be at lower risk for bone fractures compared to European and American citizens. This finding would be paradoxical, if levels of calcium consumption were the only factor determining bone density. However, Japanese studies published in 2006 and 2008 link Japan's greater levels of BMD to that country's widespread consumption of [[Nattō|natto]], a traditional breakfast dish made of fermented soybeans. Increased intake of MK-7 from natto seems to result in higher levels of activated osteocalcin and a significant reduction in fracture risk.<ref>Yaegashi Y, Onoda T, Tanno K, Kuribayashi T, Sakata K, Orimo H. (March 2008) "Association of hip fracture incidence and intake of calcium, magnesium, vitamin D, and vitamin K", ''European Journal of Epidemiology'' Vol. 23, Issue 3, pp 219-225 {{doi|10.1007/s10654-008-9225-7}}</ref><ref>[http://jn.nutrition.org/content/136/5/1323.full Ikeda et al. (May 2006) "Intake of Fermented Soybeans, ''Natto'', is Associated with Reduced Bone Loss in Postmenopausal Women: Japanese Population-Based Osteoporosis (JPOS) Study",] ''J Nutr.'' Vol.136 No.5 pp.1323-8.</ref> |
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Even more striking is the research finding, reported in 2001, that there seems to be an inverse correlation between the amount of natto consumed, in different regions of Japan, and the number of hip fractures. In regions of the country where natto is not part of the daily diet, hip fractures are more common.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/11369171 Kaneki et al. (Apr 2001) “Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of vitamin K<sub>2</sub>: possible implications for hip-fracture risk”,] ''Nutrition'' Vol.17 No.4 pp.315-21 |
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</ref> |
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===Heart calcification=== |
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Patients suffering from osteoporosis were shown to have extensive calcium plaques, which impaired blood flow in the arteries. This simultaneous excess of calcium in one part of the body (arteries), and lack in another (bones) – which may occur even in spite of calcium supplementation – is known as the Calcium Paradox. The underlying reason is vitamin K<sub>2</sub> deficiency, which leads to significant impairment in biological function of [[Matrix gla protein|MGP]], the most potent inhibitor of vascular calcification presently known. |
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Fortunately, animal research showed that vascular calcification might not only be prevented, but even reversed by increasing the daily intake of vitamin K<sub>2</sub>.<ref>[ Schurgers et al. (April 01, 2007) "Regression of warfarin-induced medial elastocal-cinosis by high intake of K vitamins in rats",] ''Blood'' Vol.109 No.7 pp.2823-2831, American Society of Hematology {{doi|10.1182/blood-2006-07-035345}}</ref> The strongly protective effect of K<sub>2</sub> and not vitamin K<sub>1</sub> on cardiovascular health was confirmed by, among others, Geleijnse et al. in the Rotterdam Study (2004, see Figure 3) performed on a group of 4,800 subjects.<ref>[ Geleijnse et al. (Nov 1, 2004) "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study",] ''J. Nutr.'' Vol.134 No.11 pp.3100-3105, The American Society for Nutritional Sciences</ref> Results of more than 10 years of follow-up were verified, also by Gast et al., who demonstrated that among K vitamins, the long-chain types of K<sub>2</sub> (MK-7 through MK-9) are the most important for efficiently preventing excessive calcium accumulation in the arteries.<ref>[ Gast et al. (Sep 2009) "A high menaquinone reduces the incidence of coronary heart disease in women",] ''Nutrition, Metabolism and Cardiovascular Diseases'' Vol.19 No.7 pp.504–510</ref><ref name=summeren>[ van Summeren et al. (Oct 2008) "Vitamin K status is associated with childhood bone mineral content",] ''[[British Journal of Nutrition]]'' Vo.100 No.4 pp.852-858 {{doi|10.1017/S0007114508921760}}</ref> |
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==Vitamin K<sub>2</sub> and children’s health== |
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Laboratory experiments, population-based studies, and clinical trials tightly link better vitamin K status to the attainment of strong and healthy bones. The beneficial role of vitamin K in children was confirmed by van Summeren et al.<ref name=summeren/> that revealed a strong positive association between vitamin K status and bone mineral content. Findings from previous studies indicated also that additional vitamin K intake may improve bone geometry and positively influence the gain in bone mass. In a study of 223 healthy girls (11–12 years), O’Connor et al.<ref>[http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=927508&fileId=S0007114507433050 O'Connor E, Mølgaard C, Michaelsen KF, Jakobsen J, Lamberg-Allardt CJ, Cashman KD. (April 2007) "Serum percentage undercarboxylated osteocalcin, a sensitive measure of K vitamins status, and its relationship to bone health indices in Danish girls",] ''British Journal of Nutrition'' Vol.97 No.4 pp.661-666 {{doi|10.1017/S0007114507433050}}</ref> found a positive relation between vitamin K status and bone mineral density. |
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Children have much higher bone metabolism than adults, so they need K vitamins in significantly larger quantities. Results from a number of studies suggest however a pronounced vitamin K deficiency in bone. In the majority of examined children, a marked elevation of undercarboxylated osteocalcin was observed, indicative for a poor K vitamin status.<ref>van Summeren M, Braam L, Noirt F, Kuis W, Vermeer C. Pronounced elevation of undercarboxylated osteocalcin in healthy children. Pediatr Res. 2007;61(3):366-70.</ref> A similar observation was made by Kalkwarf et al. showing the interdependence between vitamin K status and bone turnover.<ref>Kalkwarf HJ, Khoury JC, Bean J, Elliot JG. K vitamins, bone turnover, and bone mass in girls. Am J Clin Nutr. 2004t;80(4):1075-80.</ref> This research underlined that the requirement for K vitamins may be higher than the current recommendation, which was set in accordance only with coagulation needs. |
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==Absorption profile of different K vitamins== |
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Vitamin K is absorbed along with dietary fat from the small intestine and transported by chylomicrons in the circulation. Most of vitamin K<sub>1</sub> is carried by triacylglycerol-rich lipoproteins (TRL) and rapidly cleared by the liver; only a small amount is released into the circulation and carried by LDL and HDL. MK-4 is carried by the same lipoproteins (TRL, LDL, and HDL) and cleared fast as well. The long-chain menaquinones are absorbed in the same way as vitamin K<sub>1</sub> and MK-4, but are efficiently redistributed by the liver in predominantly LDL (VLDL). Since LDL has a long half life in the circulation, these menaquinones can circulate for extended times resulting in higher bioavailability for extra-hepatic tissues as compared to vitamin K<sub>1</sub> and MK-4. Accumulation of vitamin K in extra-hepatic tissues has direct relevance to vitamin K functions not related to hemostasis.<ref>Martin J. Shearer, Paul Newman. Metabolism and cell biology of vitamin K. Thromb Haemost 2008</ref> |
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==Dietary sources and adequate intake== |
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In 2012, Canadian health writer Kate Rhéaume-Bleue suggested the Recommended Daily Allowance (RDA) for K vitamins (range of 80-120 µg) might be too low.<ref>Kate Rhéaume-Bleue, ''Vitamin K<sub>2</sub> and the Calcium Paradox.'' Mississaugua: Wiley, 2012, p. 74.</ref> Earlier suggestions in the scientific literature, which note that the RDA is based on hepatic (i.e. related to the liver) requirements only, date back as far as 1998.<ref>Booth SL, Suttie JW. Dietary intake and adequacy of K vitamins. J Nutr. 1998;128(5):785-8.</ref><ref>Schurgers LJ, Vermeer C. Differential lipoprotein transport pathways of K-vitamins in healthy subjects. Biochim Biophys Acta. 2002;1570(1):27-32.</ref> This hypothesis is supported by the fact that the majority of the Western population exhibits a substantial fraction of undercarboxylated extra-hepatic proteins. Thus, complete activation of coagulation factors is satisfied, but there doesn’t seem to be enough vitamin K<sub>2</sub> for the carboxylation of osteocalcin in bone and MGP in the vascular system.<ref>Hofbauer LC, Brueck CC, Shanahan CM, Schoppet M, Dobnig H. Vascular calcification and osteoporosis--from clinical observation towards molecular understanding. Osteoporos Int. 2007;18(3):251-9.</ref><ref>Plantalech L, Guillaumont M, Vergnaud P, Leclercq M, Delmas PD. Impairment of gamma carboxylation of circulating osteocalcin (bone gla protein) in elderly women. J Bone Miner Res. 1991;6(11):1211-6.</ref> |
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Highest concentrations of vitamin K<sub>1</sub> are found in green leafy vegetables, but significant concentrations are also present in non-leafy green vegetables, several vegetable oils, fruits, grains and dairy. In Europe and the USA 60%, or more, of total vitamin K<sub>1</sub> intake is provided by vegetables, the majority by green leafy vegetables. National surveys reveal that K<sub>1</sub> intakes vary widely. Intakes determined by weighed-dietary Intakes are similar in mainland Britain to the USA with average daily intakes of around 70–80 μg, which is less than the adequate intake for vitamin K. Apart from animal livers, the richest dietary source of long-chain menaquinones are fermented foods (from bacteria not moulds or yeasts) typically represented by cheeses (MK-8, MK-9) in Western diets and natto (MK-7) in Japan. Food frequency questionnaire-derived estimates of relative intakes in the Netherlands suggest that ~90% of total vitamin K intakes are provided by K<sub>1</sub>, ~7.5 % by MK-5 through to MK-9 and ~ 2.5% by MK-4. Most food assays measure only fully unsaturated menaquinones; accordingly cheeses have been found to contain MK-8 at 10–20 μg/100g and MK-9 at 35–55 μg/100 g.<ref>Shearer N, Metabolism and cell biology of vitamin K. Thromb Haemost. 2008</ref> |
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==Dietary intake sources== |
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Vitamin K<sub>2</sub> is preferred by the extra-hepatic tissues (bone, cartilage, vasculature) and is of bacterial origin. Scientific discussions are ongoing as to what extent K2 produced by our intestinal bacteria contributes to our daily vitamin K<sub>2</sub> needs. If, however, intestinal bacterial supply was enough to supplement all tissues needing K2, we would not find high fractions of undercarboxylated Gla-proteins in human studies. {{citation needed|date=May 2014}}. |
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Natural K2 is also found in bacterial fermented foods, like mature cheeses and curd. The MK-4 form of K2 is often found in relatively small quantities in meat and eggs. The richest source of Natural K2 is the traditional Japanese dish [[Nattō|natto]]<ref>Kaneki M, Hodges SJ, Hosoi T, Fujiwara S, Lyons A, Crean SJ, Ishida N, Nakagawa M, Takechi M, Sano Y, Mizuno Y, Hoshino S, Miyao M, Inoue S, Horiki K, Shiraki M, Ouchi Y, Orimo H; ''Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of K vitamins2: possible implications for hip-fracture risk''; Nutrition; 2001; 17(4): 315-321.</ref> made of fermented soybeans and ''[[Bacillus subtilis]]'', which provides an unusually rich source of Natural K2 as long-chain MK-7: its consumption in [[North Japan]] has been linked to significant improvement in K vitamin's status and bone health in many studies. The intense smell and strong taste, however, make this soyfood a less attractive source of Natural K2 for Westerners' tastes, but supplement food companies sell nattō in capsules. It is not known whether ''B. Subtilis'' will produce K2 with other legumes ([[chickpeas]], [[beans]], [[lentils]]). |
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==Other sources== |
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Accumulating evidence suggests that Western society is affected by subclinical deficiency of vitamin K. Moreover, it has been scientifically proven that for optimal bone and vascular health, relatively high in-takes of vitamin K are required. {{citation needed|date=March 2013}} |
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The synthetic (and less effective) short-chain vitamin K<sub>1</sub> is commonly used in food supplements. In case of vitamin K<sub>2</sub>, the most popular forms are MK-4 and MK-7. |
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==Vitamin K deficiency== |
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{{One source|section|date=September 2014}} |
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There are two kinds of vitamin K deficiency: acute and chronic. |
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Widely recognized, acute deficiency is characterized by unusual bleeding from gums, nose, or the gastrointestinal tract. Consequences can be severe, including internal clogging, strokes, lung damage, and death caused by immoderate blood loss. |
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Newborn infants are at increased risk for acute vitamin K deficiency, because vitamin K is not transported sufficiently across the placenta, and the newborn gut is sterile at the beginning. Thus, there are no bacteria to produce the required amount of vitamin K. |
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Vitamin K deficiency may also occur with the use anticoagulant drugs (i.e., warfarin or other coumarins), prolonged use of antibiotics, gallbladder disease, and Crohn’s disease. |
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Chronic vitamin K deficiency is less obvious than acute deficiency. It is actually more dangerous because there are no alarming symptoms and the results - impairments in bone, cardiovascular health, and other disease of aging – might be severe. |
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It had been long believed that vitamin K deficiency is rare. Requirements could be easily met via diet and microbial biosynthesis by bacteria living in the gut. However, recent scientific data show that the amount of vitamin K is not as abundant in the diet as once thought. Even a well-balanced diet might not provide vitamin K in the amounts sufficient for satisfying the body’s needs. This is especially concerning given that, according to researcher CJ Prynne, mean dietary intake of vitamin K is currently significantly lower than it was 50 years ago, while the daily consumption of vitamin K has gradually decreased since 1950.<ref>Prynne CJ, Thane CW, Prentice A, Wadsworth ME. Intake and sources of phylloquinone (vitamin K(1)) in 4-year-old British children: comparison between 1950 and the 1990s. Public Health Nutr. 2005;8(2):171-80.</ref> |
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This shortage can be partly explained by alterations in food composition (people eat much less green-leafy vegetables, which are rich in vitamin K<sub>1</sub>) and different preparation practices. Food used to be made in the presence of various bacteria species (synthesizing vitamin K<sub>2</sub>). Now, sterile conditions introduced by international standards of food manufacturing stop microorganisms, including beneficial flora, from multiplying and penetrating the human body. |
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Dietary patterns have also changed over decades. For example, children in 1950 derived around 15% of their vitamin K intake from fats and oil sources and 55% from vegetables (excluding potatoes). In the 1990s, 35% came from fats and oils, and just 30% from vegetables. |
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Moreover, it was shown that all K vitamins are absorbed from the gastrointestinal tract in the small intestine. Bacterial colonies producing menaquinones are located in the colon (large intestine), where the bile salts required for vitamin K uptake are not present. As stated earlier, the efficacy of intestinal vitamin K absorption might be questionable. Further, the presently used Recommended Dietary Intake for vitamin K might be too low. The need for complete activation of coagulation factors is satisfied, but it's not enough to fulfill all of vitamin K's benefits. |
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==Vitamin K status== |
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Measurement techniques: |
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* Food frequency questionnaires to determine vitamin K intake. Disadvantage = Rough estimates |
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* Circulating vitamin K levels |
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* Biomarker to reflect vitamin K sufficiency |
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High-performance liquid chromatography is the technique to measure the level of vitamin K in the blood. Disadvantage = However, circulating vitamin K levels correspond to the daily intake of green-leafy vegetables, cheeses, etc. |
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The best way to evaluate vitamin K deficiency is to determine the decrease in the circulating undercarboxylated form of the vitamin K-dependent proteins in the blood (e.g., the level of carboxylated osteocalcin or MGP). |
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==Anticoagulants and K<sub>2</sub> supplementation== |
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Recent studies found a clear association between long-term anticoagulant treatment (OAC) and reduced bone quality due to reduction of active osteocalcin. OAC might lead to an increased incidence of fractures, reduced bone mineral density/bone mineral content, osteopenia, and increased serum levels of undercarboxylated osteocalcin.<ref>Caraballo PJ, Gabriel SE, Castro MR, Atkinson EJ, Melton LJ 3rd. Changes in bone density after exposure to oral anticoagulants: a meta-analysis.Osteoporos Int. 1999;9(5):441-8.</ref> Bone mineral density was significantly lower in stroke patients with long-term warfarin treatment compared to untreated patients and osteopenia was probably an effect of warfarin-interference with vitamin K recycling.<ref>Sato Y, Honda Y, Kunoh H, Oizumi K. Long-term oral anticoagulation reduces bone mass in patients with previous hemispheric infarction and nonrheumatic atrial fibrillation. Stroke. 1997;28(12):2390-4.</ref> |
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Furthermore, OAC is often linked to an undesired soft-tissue calcification in both children and adults.<ref>Barnes C, Newall F, Ignjatovic V, Wong P, Cameron F, Jones G, Monagle P. Reduced bone density in children on long-term warfarin. Pediatr Res. 2005;57(4):578-81.</ref><ref>Hawkins D, Evans J. Minimising the risk of heparin-induced osteoporosis during pregnancy. Expert Opin Drug Saf. 2005;4(3):583-90</ref> This process has been shown to be dependent upon the action of K vitamins. Vitamin K deficiency results in undercarboxylation of MGP. Vascular calcification was shown to appear in warfarin-treated experimental animals within two weeks.<ref>Price PA, Faus SA, Williamson MK. Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves. Arterioscler Thromb Vasc Biol. 1998;18(9):1400-7.</ref> Also in humans on OAC treatment, two-fold more arterial calcification was found as compared to patients not receiving vitamin K antagonists.<ref>Schurgers LJ, Aebert H, Vermeer C, Bültmann B, Janzen J. Oral anticoagulant treatment: friend or foe in cardiovascular disease? Blood. 2004 15;104(10):3231-2.</ref><ref>Koos R, Mahnken AH, Mühlenbruch G, Brandenburg V, Pflueger B, Wildberger JE, Kühl HP. Relation of oral anticoagulation to cardiac valvular and coronary calcium assessed by multislice spiral computed tomography. Am J Cardiol. 2005;96(6):747-9.</ref> Among consequences of anticoagulant treatment: increased aortic wall stiffness, coronary insufficiency, ischemia, and even heart failure. Arterial calcification might also contribute to systolic hypertension and ventricular hypertrophy.<ref>Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol. 2005;25(5):932-43.</ref><ref>Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of coronary artery calcium screening in subjects with and without diabetes. J Am Coll Cardiol. 2004;43(9):1663-9.</ref> Coumarins, by interfering with vitamin K metabolism, might also lead to an excessive calcification of cartilage and tracheobronchial arteries. |
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Anticoagulant therapy is usually instituted to avoid life-threatening diseases and a high vitamin K intake interferes with the anticoagulant effect. Patients on [[warfarin]] (Coumadin) treatment, or treatment with other [[vitamin K antagonist]] drugs, are therefore advised not to consume diets rich in K vitamins. However, the latest research proposed to combine vitamins K with OAC to stabilize the INR (International normalized ratio, a laboratory test measure of blood coagulation). |
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== Toxicidad == |
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No se conocen efectos tóxicos asociados con altas dosis de menaquinonas. Los individuos que se encuentran tomando medicaciones anticoagulantes tales como la [[warfarina]] ([[cumarina]]s) deberían consultar con su médico antes de tomar vitamina {{fquim|K|2}}. A diferencia de otras vitaminas liposolubles, la vitamina K no se almacena en cantidad significativa en el hígado; por lo que no se han descrito niveles tóxicos. Doda los datos disponibles hasta el momento demuestran que la vitamina K no presenta efectos adversos en sujetos saludables. Se han publicado recientemente las recomendaciones para la ingesta diaria de vitamina K, coincidiendo además con el amplio margen de seguridad de la vitamina K: «''Una búsquda en la literatura no revela evidencias de toxicidad asociada con la ingesta de vitamina {{fquim|K|1}} ni {{fquim|K|2}}''». Sin embargo un punto de atención es la potencial interferencia de las vitaminas K con los tratamientos anticoagulantes orales. Los modelos animales, si son generalizables a humanos, muestran que MK-7 tiene una buena tolerancia.<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172146/ Pucaj et al. (Sep 2011) "Safety and toxicological evaluation of a synthetic vitamin K2, menaquinone-7",] ''Toxicology Mechanisms and Methods'' Vol.21 No.7 pp.520–532</ref> |
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== Referencias == |
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{{Reflist}} |
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== Enlaces externos == |
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* [http://www.vitak.com/ Vitak BV - a research company with a long expertise in all aspects of vitamin K and vitamin K-dependent proteins] |
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* [http://www.vitamink2.org/ VitaminK2.org - an international community founded to explore and understand the emerging role of Natural Vitamin K<sub>2</sub> in human health] |
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* [http://www.menaquingold.com/ MenaquinGold - a natural vitamin k2-7 product manufactured by a BioPharma company with high expertise in manufacturing natural vitamin k2-7 ] |
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[[Categoría:Vitaminas]] |
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Revisión del 21:57 19 mar 2015
Las menaquinonas o vitaminas K
2, es el nombre de grupo dado a una familia de compuestos relacionados, generalmente divididos en menaquinonas de cadena corta (de la cual la menatetrenona o MK-4, es el miembro más importante), y las menaquinonas de cadena larga, de las cuales MK-7, MK-8 y MK-9 son las más reconocidas desde el punto de vista nutricional.
Formas
2.
Todas las vitaminas K son similares en estructura; comparten un núcleo formado por un anillo quinona, pero difieren en la longitud y grado de saturación de la cola carbonada y del número de cadenas laterales que esta posee.[1] El número de cadenas laterales se encuentra indicado en el nombre particular de cada menaquinona (por ejemplo, MK-4 significa que cuatro unidades moleculares de tipo isopreno se encuentran unidas a la cola carbonada), y esto influencia el transporte a diferentes tejidos diana.
Mecanismo de acción
El mecanismo de acción de la vitamina K
2 es similar al de la vitamina K
1. Tradicionalmente, las vitaminas K son reconocidas como un factor requerido para la coagulación, pero las funciones desempeñadas por este grupo de vitaminas se revela mucho más complejo. Las vitaminas K desempeñan un papel esencial como cofactor de la enzima gama-glutamil carboxilasa, la cual se encuentra involucrada en la carboxilación de las proteínas dependientes de vitamina K, esto es la conversión de los ácidos glutámicos (Glu) que forman parte de un péptido, a ácido γ-carboxi glutámico (Gla).
.
La carboxilación de proteínas dependientes de vitamina K, conocidas como Proteínas Gla, es un proceso importante y sirve como vía de reciclaje para recuperar a la vitamina K de sus metabolitos de tipo epóxido (K0) para su reutilización en carboxilaciones. Se han descubierto varias proteínas humanas que contienen el dominio Gla y que son sintetizadas en diferentes tipos de tejidos:
- Factores de la coagulación (II, VII, IX, X), como así también las proteínas anticoagulantes (C, S, Z). Estas proteínas Gla se sintetizan en el hígado y desempeñan un importante papel en la homeostasis sanguínea.
- Osteocalcina. Esta proteína no colágena es secretada por los osteoblastos y desempeña un papel primordial en la mineralización del hueso.
- Proteína Gla matriz (MGP). Esta proteína inhibidora de la calcificación, se encuentra en numerosos tejidos, pero su papel más importante lo desempeña en cartílago y paredes de vasos arteriales.
- Proteína específica de detención del crecimiento 6 (GAS6). La GAS6 se secreta en los linfocitos y células endoteliales en respuesta al daño y ayuda a la supervivencia celular, proliferación, migración y adhesión.
- Proteínas Gla ricas en prolina (PRGP), proteínas Gla transmembrana (TMG) y periostina (GRP), cuya función precisa aún no ha sido explorada.
Toxicidad
No se conocen efectos tóxicos asociados con altas dosis de menaquinonas. Los individuos que se encuentran tomando medicaciones anticoagulantes tales como la warfarina (cumarinas) deberían consultar con su médico antes de tomar vitamina K
2. A diferencia de otras vitaminas liposolubles, la vitamina K no se almacena en cantidad significativa en el hígado; por lo que no se han descrito niveles tóxicos. Doda los datos disponibles hasta el momento demuestran que la vitamina K no presenta efectos adversos en sujetos saludables. Se han publicado recientemente las recomendaciones para la ingesta diaria de vitamina K, coincidiendo además con el amplio margen de seguridad de la vitamina K: «Una búsquda en la literatura no revela evidencias de toxicidad asociada con la ingesta de vitamina K
1 ni K
2». Sin embargo un punto de atención es la potencial interferencia de las vitaminas K con los tratamientos anticoagulantes orales. Los modelos animales, si son generalizables a humanos, muestran que MK-7 tiene una buena tolerancia.[2]
Referencias
- ↑ Shearer MJ.2003 in Physiology. Elsevier Sciences LTD. 6039-45.
- ↑ Pucaj et al. (Sep 2011) "Safety and toxicological evaluation of a synthetic vitamin K2, menaquinone-7", Toxicology Mechanisms and Methods Vol.21 No.7 pp.520–532
Enlaces externos
- Vitak BV - a research company with a long expertise in all aspects of vitamin K and vitamin K-dependent proteins
- VitaminK2.org - an international community founded to explore and understand the emerging role of Natural Vitamin K2 in human health
- MenaquinGold - a natural vitamin k2-7 product manufactured by a BioPharma company with high expertise in manufacturing natural vitamin k2-7