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Vitamin K2

Vitamin K2(20) (MK-4) menaquinon-4   Product Code:  185834

Vitamin K2(35) (MK-7) Menaquinon-7   Product Code:  185837

Vitamin K2(45) (MK-9) Menaquinon-9   Product Code:  185838

 

vitamin K2(20) 500 g
0.13% Oil
1.3% Oil
0.13% Power
1.3% Power            270 €
98.0% Oil            5.150 €
98.0% Power       5.860 €

Vitamin K2(35)
0.13% Oil
1.3% Oil           1.198 €
0.13% Power       191 €
1.3% Power      1.598 €

Vitamin K2(45)
0.13% Power
1.3% Power
98.0% Power       5.250 €

 

 

Getting to Know Vitamin K2 and its Effects

The Special Effects of Vitamin K2

1.      Curing haemorrhage caused by VK2 deficiency; promotes the formation of thrombin, accelerates blood clotting, maintains proper clotting time; also used as quick coagulant in surgeries or first aids

2.      Curing and preventing osteoporosis; VK2 produces a specific protein known as osteocalcin which can bind calcium, therefore to increase the density of bones and to prevent fracture. 

3.      Prevention of hepatocellular carcinoma in women with viral cirrhosis.

4.      function of diuresis, promoting the detoxifcation of liver and lowering the blood pressure. 

 

Menaquinone (Vitamin K2)

Vitamin K is found in plants as phylloquinone (vitamin K1) and in animals as menaquinone (vitamin K2).

Vitamin K2 is essential for the carboxylation of glutamate residues in certain proteins, to give -carboxyglutamate. This modification allows the protein to bind calcium, an essential event in the blood clotting cascade. Carboxylation of glutamate is also important in other proteins involved in the mobilization or transport of calcium.

Vitamin K exists in two forms, K1 and K2. Both vitamins are coenzymes of gammaglutamyl carboxylase and are thus able to regulate mineralization of bone and calcification of blood vessels. Vitamin K2 however is more effective than vitamin K1 with respect to osteoclastogenesis likewise hypocholesterolemic effects and the ability to slow atherosclerotic progression have only been observed with vitamin K2. This may be due in part to the geranylgeranyl side chain of vitamin K2 which is thought to inhibit the mevalonate pathway, thus preventing the prenylation of growth factors required for osteoclast activation in much the same way as nitrogen-containing bisphosphonates. This therefore suggests that modelling of vitamin K2 may lead to the development of therapeutic candidates able to reduce resorption, increase bone mineralization and limit atherosclerosis. Furthermore, targeting vitamin K2 over vitamin K1 may be confer beneficial pharmacokinetics given that vitamin K1 concentrates in the liver while vitamin K2 is well distributed to bone and blood vessel walls. Equally, this profile is expected to limit the primary adverse effect associated with vitamin K, negative interactions with coumarin anti-coagulants, since the proteins involved in coagulation are primarily synthesized in the liver.

Vitamin K2 is the collective term for a group of vitamin K compounds called menaquinones. The menaquinone homolgues are characterized by the number of isoprene residues comprising the side chain. The side chain is located at position 3 of the naphthoquinone ring. The group chemical name of the menaquinones is 2-methyl-3-all-trans-polyprenyl-1, 4-naphthoquinones. Menaquinones with side chains of up to 15 isoprene units have been described. Menaquinones of from two to 13 isoprene units have been found in human and animal tissues. Menaquinones are designated by the name menaquinone followed by a number. The number refers to the number of isoprene residues in the structure. Thus, menaquinone-4, abbreviated MK-4, possesses four isoprene residues in the side chain. Menaquinone-7 possesses seven isoprene units in the side chain. The menaquinones may also be designated by the number of carbons in the side chain. An isoprene residue contains five carbons. Thus, menaquinone-4 is also called vitamin K2 (20) and menaquinone-7 is also called vitamin K2 (35). Menaquinone-4 is also known as menatetrenone. The fermented soybean product natto is rich in menaquinone-7. Menaquinone-4 is the predominant form of vitamin K in the rat brain.

Research History of Vitamin K2

In 1934, Danish scientist, Dr. Henrik Dam discovered vitamin K and approved as fat-soluble vitamin. Vitamin K1, or phylloquinone, is found naturally in plants. Vitamin K2, also called menaquinone, is made by the bacteria that line the gastrointestinal tract.

 

Vitamin K is one of indispensable vitamins in body, can rapidly amend bleeding caused by lack of VK, it has been used as coagulant for several decades but not noted as an important bodily nutriment. The many other benefits of vitamin K are often overlooked.

 

Howeverin recent 40 years, especially in recent 20 years, research proved that vitamin K2 plays a crucial role in many bodily functions. Vitamin K2 involves in bone metabolism and is important for maintaining high bone densities and boots bone health. Vitamin K's usefulness against osteoporosis and heart disease is now becoming too abundant to overlook. In addition, vitamin K2 has the function of prevention of hepatocellular carcinoma in female patients with viral cirrhosis. It is also a stronger antioxidant than vitamin E or coenzyme Q10it may be a key anti-aging vitamin as well. Japanese researchers found that vitamin K2 deficiency can have effects similar to diabetes .And now, scientists are even looking at vitamin K2 to be the future of treating certain kinds of cancer and Alzheimer's disease.

Application Prospect on Vitamin K2

 

1.       Vitamin K2, The Pinnacle of Bone Health What is Osteoporosis?

As defined by the World Health Organization, osteoporosis is a generalized skeletal disorder of low bone mass (thinning of the bone) and deterioration in its architecture, causing susceptibility to fracture. If not prevented or if left untreated, osteoporosis can progress painlessly until a bone breaks. These broken bones, also known as fractures, occur typically in the hip, spine, and wrist.

Any bone can be affected, but of special concern are fractures of the hip and spine. A hip fracture almost always requires hospitalization and major surgery. It can impair a person's ability to walk unassisted and may cause prolonged or permanent disability or even death. Spinal or vertebral fractures also have serious consequences, including loss of height, severe back pain, and deformity.

What Causes Osteoporosis?

From infancy through our late twenties we add minerals, particularly calcium, to the inner cores of our bones, strengthening them. After the age of 30, we lose more minerals than we add. Osteoporosis affects both men and women as they age. There are several causes lead to osteoporosis:

1). Postmenopausal osteoporosis (Type I osteoporosis)  generally develops in women after menopause when the amount of estrogen in the body greatly decreases. This process leads to an increase in the resorption of bone (the bones loses substance).

2). Senile osteoporosis (Type II osteoporosis) typically happens after the age of 70 and affects women twice as frequently as men. While women are four times more likely than men to develop the disease, men also suffer from osteoporosis.

3). Heredity and lifestyle can hasten the process of losing minerals. Whites and Asians, tall and thin people, and those with a family history of osteoporosis are at the highest risk. While women develop osteoporosis younger than men, men are not immune. Behavioral factors that increase the risk of osteoporosis and osteoporotic fractures include smoking, alcohol abuse, a diet low in calcium, too little exposure to sunlight (necessary for Vitamin D metabolism and stronger bones) and prolonged inactivity.

4).  A number A number of diseases, many associated with aging, can also cause osteoporosis. These include kidney failure, cancers, liver disease, Paget's disease, endocrine or glandular diseases, rheumatoid arthritis and gonadal failure (such as from surgical removal of the testes or ovaries). Medications, including steroids, thyroid hormone, seizure drugs and blood thinners, can also cause osteoporosis.

Risk Factors

Certain people are more likely to develop osteoporosis than others.  Factors that increase the likelihood of developing osteoporosis and fractures are called "risk factors."  These risk factors include: 

  • Personal history of fracture after age 50
  • Current low bone mass
  • History of fracture in a 1?relative
  • Being female
  • Being thin and/or having a small frame
  • Advanced age
  • A family history of osteoporosis
  • Estrogen deficiency as a result of menopause, especially early or surgically induced
  • Abnormal absence of menstrual periods (amenorrhea)
  • Anorexia nervosa
  • Low lifetime calcium intake
  • Vitamin D deficiency
  • Use of certain medications (corticosteroids, chemotherapy, anticonvulsants and others)
  • Presence of certain chronic medical conditions
  • Low testosterone levels in men
  • An inactive lifestyle
  • Current cigarette smoking
  • Excessive use of alcohol
  • Being Caucasian or Asian, although African Americans and Hispanic Americans are at significant risk as well

Prevention : Menaquinone (Vitamin K2) cures and prevents osteoporosis:

Although there is no cure for osteoporosis, building strong bones during childhood and adolescence can be the best defense against developing osteoporosis later. Vitamin K2— a new way that an optimize bone health and help prevent osteoporosis. 

Vitamin K2 Regulation of Bone Homeostasis Is Mediated by the Steroid and Xenobiotic Receptor SXR*

Michelle M. Tabb, Aixu Sun, Changcheng Zhou, Felix Grün, Jody Errandi, Kimberly Romero, Hang Pham, Satoshi Inoue, Shyamali Mallick, Min Lin, Barry M. Forman, and Bruce Blumberg

From the {ddagger}Department of Developmental and Cell Biology, University of California, Irvine, California 92697-2300, the Department of Geriatric Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan, and the Division of Molecular Medicine, Gonda Diabetes Research Center, Beckman Research Institute, The City of Hope National Medical Center, Duarte, California 91010-3000

Vitamin K2 is a critical nutrient required for blood clotting that also plays an important role in bone formation. Vitamin K2 supplementation up-regulates the expression of bone markers, increases bone density in vivo, and is used clinically in the management of osteoporosis. The mechanism of vitamin K2 action in bone formation was thought to involve its normal role as an essential cofactor for {gamma}-carboxylation of bone matrix proteins. However, there is evidence that suggests vitamin K2 also has a transcriptional regulatory function. Vitamin K2 bound to and activated the orphan nuclear receptor SXR and induced expression of the SXR target gene, CYP3A4, identifying it as a bona fide SXR ligand. Vitamin K2 treatment of osteosarcoma cells increased mRNA levels for the osteoblast markers bone alkaline phosphatase, osteoprotegerin, osteopontin, and matrix Gla protein. The known SXR activators rifampicin and hyperforin induced this panel of bone markers to an extent similar to vitamin K2. Vitamin K2 was able to induce bone markers in primary osteocytes isolated from wild-type murine calvaria but not in cells isolated from mice deficient in the SXR ortholog PXR. We infer that vitamin K2 is a transcriptional regulator of bone-specific genes that acts through SXR to favor the expression of osteoblastic markers. Thus, SXR has a novel role as a mediator of bone homeostasis in addition to its role as a xenobiotic sensor. An important implication of this work is that a subset of SXR activators may function as effective therapeutic agents for the management of osteoporosis.

Effects of vitamin K2 on osteoporosis

Vitamin K2 is a cofactor of gamma-carboxylase, which converts the glutamic acid (Glu) residue in osteocalcin molecules to gamma-carboxyglutamic acid (Gla), and is, therefore, essential for gamma-carboxylation of osteocalcin. Available evidence suggests that vitamin K2 also enhances osteocalcin accumulation in the extracellular matrix of osteoblasts in vitro. Osteocalcin-knockout mice develop hyperostosis, suggesting that the Gla-containing osteocalcin promotes normal bone mineralization. Although the precise role of osteocalcin in bone mineralization remains obscure, it probably regulates the growth of hydroxyapatite crystals. Furthermore, vitamin K2 also inhibits the expression of the osteoclast differentiation factor (ODF)/RANK ligand, tartrate-resistant acid phosphatase activity, and mononuclear cell formation, and induces osteoclast apoptosis in vitro. There is some evidence indicating that vitamin K2 prevents bone resorption in ovariectomized rats, retards the increase in bone turnover in orchidectomized rats, ameliorates the increase in bone resorption and decrease in bone formation in sciatic neurectomized rats, and prevents the decrease in bone formation in glucocorticoid-treated rats. These findings suggest that vitamin K2 may not only stimulate bone formation but also suppress bone resorption in vivo. Clinically, vitamin K2 sustains the lumbar bone mineral density (BMD) and prevents osteoporotic fractures in patients with age-related osteoporosis, prevents vertebral fractures in patients with glucocorticoid-induced osteoporosis, increases the metacarpal BMD in the paralytic upper extremities of patients with cerebrovascular disease, and sustains the lumbar BMD in patients with liver-dysfunction-induced osteoporosis. Vitamin K deficiency, as indicated by an increased circulating level of undercarboxylated osteocalcin, may contribute to osteoporotic fractures. Even though the effect of vitamin K2 on the BMD is quite modest, this vitamin may have the potential to regulate bone metabolism and play a role in reducing the risk of osteoporotic fractures. No randomized well-controlled prospective studies conducted on a sufficiently large number of patients have been reported yet, therefore, further studies are needed to confirm the efficacy of vitamin K2 in the treatment of osteoporosis.

Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis.

Research Institute and Practice for Involutional Diseases, Nagano Prefecture, Japan.

Attempting to investigate whether vitamin K2 (menatetrenone) treatment effectively prevents the incidence of new fractures in osteoporosis. A total of 241 osteoporotic patients were enrolled in a 24-month randomized open label study. The control group (without treatment; n = 121) and the vitamin K2-treated group (n = 120), which received 45 mg/day orally vitamin K2, were followed for lumbar bone mineral density (LBMD; measured by dual-energy X-ray absorptiometry [DXA]) and occurrence of new clinical fractures. Serum level of Glu-osteocalcin (Glu-OC) and menaquinone-4 levels were measured at the end of the follow-up period. Serum level of OC and urinary excretion of deoxypyridinoline (DPD) were measured before and after the treatment. The background data of these two groups were identical. The incidence of clinical fractures during the 2 years of treatment in the control was higher than the vitamin K2-treated group (chi2 = 10.935; p = 0.0273). The percentages of change from the initial value of LBMD at 6, 12, and 24 months after the initiation of the study were -1.8 +/- 0.6%, -2.4 +/- 0.7%, and -3.3 +/- 0.8% for the control group, and 1.4 +/- 0.7%, -0.1 +/- 0.6%, and -0.5 +/- 1.0% for the vitamin K2-treated group, respectively. The changes in LBMD at each time point were significantly different between the control and the treated group (p = 0.0010 for 6 months, p = 0.0153 for 12 months, and p = 0.0339 for 24 months). The serum levels of Glu-OC at the end of the observation period in the control and the treated group were 3.0 +/- 0.3 ng/ml and 1.6 +/- 0.1 ng/ml, respectively (p < 0.0001), while the serum level of OC measured by the conventional radioimmunoassay (RIA) showed a significant rise (42.4 +/-6.9% from the basal value) in the treated group at 24 months (18.2 +/- 6.1% for the controls;p = 0.0081). There was no significant change in urinary DPD excretion in the treated group. These findings suggest that vitamin K2 treatment effectively prevents the occurrence of new fractures, although the vitamin K2-treated group failed to increase in LBMD. Furthermore, vitamin K2 treatment enhances gamma-carboxylation of the OC molecule

2.Medical effects-Curing haemorrhage caused by VK2 deficiency:

Vitamin K is necessary for normal coagulation (blood clotting) and prophylaxis for neonatal vitamin K deficient intracranial haemorrhage. Vitamin K2 is the biologically active substances in animals, and vitammin K1 and vitamin K3 must need to translate into vitamin K3 to have active effects. These three forms of vitamin K all translate into vitamin K2 in the liver, and are absorbed with vitamin K2 synthesized by bacteria in the gastrointestinal tract. Mankind is barely to have original vitamin deficiency except newborn infants. Infants of 1-2 weeks age, often have low thrombin that is because the placenta is difficult to transport fat. Thrombin in infants’ body raise to normal rate in several weeks, whereas, newborn infants will have haemorrhage disease if their thrombin rate is lower than normal rate by 10%. Water-soluble or fat-soluble vitamin K2 preparation can get thrombin back to normal rate and control the bleeding efficiently. Long thrombin time sometimes occur in some senior citizens because they may lack of vitamin K2. Also patients have decrease of thrombin when they take certain type of drugs such as dicarboxylic coumarin, then a prevention of this disease should be achieved by venous injection of vitamin K2.

 

3.Prevention of hepatocellular carcinoma in women with viral cirrhosis.

Role of Vitamin K2 in the Development of Hepatocellular Carcinoma in Women With Viral Cirrhosis of the Liver

Context: Previous findings indicate that vitamin K2 (menaquinone) may play a role in controlling cell growth.

Objective:  To determine whether vitamin K2has preventive effects on the development of hepatocellular carcinoma in women with viral cirrhosis of the liver.

Design, Setting, and Participants:  Forty women diagnosed as having viral liver cirrhosis were admitted to a university hospital between 1996 and 1998 and were randomly assigned to the treatment or control group. The original goal of the trial was to assess the long-term effects of vitamin K2 on bone loss in women with viral liver cirrhosis. However, study participants also satisfied criteria required for examination of the effects of such treatment on the development of hepatocellular carcinoma.

Interventions:  The treatment group received 45 mg/d of vitamin K2 (n = 21). Participants in the treatment and control groups received symptomatic therapy to treat ascites, if necessary, and dietary advice.

Main Outcome Measure:  Cumulative proportion of patients with hepatocellular carcinoma.

Results:  Hepatocellular carcinoma was detected in 2 of the 21 women given vitamin K2 and 9 of the 19 women in the control group. The cumulative proportion of patients with hepatocellular carcinoma was smaller in the treatment group (log-rank test, P = .02). On univariate analysis, the risk ratio for the development of hepatocellular carcinoma in the treatment group compared with the control group was 0.20 (95% confidence interval [CI], 0.04-0.91; P = .04). On multivariate analysis with adjustment for age, alanine aminotransferase activity, serum albumin, total bilirubin, platelet count, {alpha}-fetoprotein, and history of treatment with interferon alfa, the risk ratio for the development of hepatocellular carcinoma in patients given vitamin K2 was 0.13 (95% CI, 0.02-0.99; P = .05).

Conclusion:  There is a possible role for vitamin K2 in the prevention of hepatocellular carcinoma in women with viral cirrhosis.

Detailed Information on Specifications of MK-4MK7MK-9

1. Vitamin K2(20) (MK-4) menaquinon-4   Product Code:  185834

MK-4

 

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Last modified: 05/29/09