Vitamin K2 | MK-7 | Menaquinone 7
Vitamin K is a collective term for a group of structurally related fat-soluble molecules (vitamers) that act as a cofactor for a carboxylase enzyme. This enzyme transforms glutamate residues in proteins to carboxyglutamate residues, which plays an important role in blood clotting and bone health. Dietary vitamin K1 (phylloquinone) is obtained from vegetables, whereas dietary vitamin K2 (menaquinone) is obtained from products of animal origin or bacterial fermentation (e.g., cheese, natto). Vitamin K2 can also be produced by gut bacteria from vitamin K1. There are nine related vitamin K2 compounds—MK-1, MK-2 ... MK-9. The M stands for menaquinone, the K stands for vitamin K, and the n represents the number of isoprenoid side chain residues. In general, vitamin K2 is the preferred form for supporting bone and vascular health.
Menaquinone-7 (MK-7) is a bioavailable vitamin K2, needing much lower doses than MK-4.
Produced from natto and manufactured by Japan Bioscience Labs (JBSL), a leading Japanese natto manufacturer for decades.
A clinically studied form of vitamin K2 which has been used in studies lasting up to three years.
Non-GMO, Vegan, Gluten Free
The dose of vitamin K needed will depend on the use and the form used. Of the available forms of vitamin K2, in general, shorter chain forms (MK-4, -5, and -6) require much higher doses than the longer-chain MK-7. Depending on the purpose the amount of vitamin K2 supplemented can vary (i.e., a higher dose would be used to optimize bone health, while a lower dose would be used if its an ingredient intended to support mitochondrial function).
Mitochondrial structure and function
Exercise performance (ergogenic effect)
1. S. Eleff et al., Proc. Natl. Acad. Sci. U. S. A. 81, 3529–3533 (1984).
2. Z. Argov et al., Ann. Neurol. 19, 598–602 (1986).
3. M. Vos et al., Science. 336, 1306–1310 (2012).
4. V. Shneyvays, D. Leshem, Y. Shmist, T. Zinman, A. Shainberg, J. Mol. Cell. Cardiol. 39, 149–158 (2005).
5. F. A. Wijburg, C. J. de Groot, N. Feller, R. J. Wanders, J. Inherit. Metab. Dis. 14, 293–296 (1991).
6. J. M. Cooper, D. J. Hayes, R. A. Challiss, J. A. Morgan-Hughes, J. B. Clark, Brain. 115 ( Pt 4), 991–1000 (1992).
7. F. A. Wijburg, N. Feller, C. J. de Groot, R. J. Wanders, Biochem. Int. 22, 303–309 (1990).
8. N. K. Isaev, E. V. Stelmashook, K. Ruscher, N. A. Andreeva, D. B. Zorov, Neuroreport. 15, 2227–2231 (2004).
9. T. S. Chan et al., Free Radic. Res. 36, 421–427 (2002).
10. W. W. Anderson, R. D. Dallam, J. Biol. Chem. 234, 409–411 (1959).
11. R. E. Beyer, J. Biol. Chem. 234, 688–692 (1959).
12. C. E. Horth et al., Biochem. J. 100, 424–429 (1966).
13. Y.-X. Yu et al., Acta Pharmacol. Sin. 37, 1178–1189 (2016).
14. L. M. Baldoceda-Baldeon, D. Gagné, C. Vigneault, P. Blondin, C. Robert, Reproduction. 148, 489–497 (2014).
15. H. J. Choi et al., Diabetes Care. 34, e147 (2011).
16. M. Yoshida et al., Diabetes Care. 31, 2092–2096 (2008).
17. N. Sakamoto, T. Nishiike, H. Iguchi, K. Sakamoto, Clin. Nutr. 19, 259–263 (2000).
18. A. G. Hussein, R. H. Mohamed, S. M. Shalaby, D. M. Abd El Motteleb, Nutrition. 47, 33–38 (2018).
19. Y. Li, J. P. Chen, L. Duan, S. Li, Diabetes Res. Clin. Pract. 136, 39–51 (2018).
20. B. K. McFarlin, A. L. Henning, A. S. Venable, Altern. Ther. Health Med. 23, 26–32 (2017).
21. D. S. Mehta et al., The Indian Practitioner. 63, 287–291 (2010).
22. T. Krueger, R. Westenfeld, L. Schurgers, V. Brandenburg, Int. J. Artif. Organs. 32, 67–74 (2009).
23. J. W. J. Beulens et al., Br. J. Nutr. 110, 1357–1368 (2013).
24. Y. Zhang et al., Oncotarget. 8, 24719–24727 (2017).
25. H. Zhang et al., Oncol. Rep. 25, 159–166 (2011).
26. J. Li et al., J. Neurosci. 23, 5816–5826 (2003).
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