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Vitamin K is a family of structurally similar, fat-soluble vitamers found in foods and marketed as dietary supplements. [1] The human body requires vitamin K for post-synthesis modification of certain proteins that are required for blood coagulation ("K" from Danish koagulation, for "coagulation") or for controlling binding of calcium in bones and other tissues. [2]
Vitamin K 2 or menaquinone (MK) (/ ˌ m ɛ n ə ˈ k w ɪ n oʊ n /) is one of three types of vitamin K, the other two being vitamin K 1 (phylloquinone) and K 3 . K 2 is both a tissue and bacterial product (derived from vitamin K 1 in both cases) and is usually found in animal products or fermented foods .
This was followed in the 1950s by the mass production and marketing of vitamin supplements, including multivitamins, to prevent vitamin deficiencies in the general population. [8] Governments have mandated the addition of some vitamins to staple foods such as flour or milk, referred to as food fortification , to prevent deficiencies. [ 9 ]
The pathway produces two five-carbon building blocks called isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate (DMAPP), which are used to make isoprenoids, a diverse class of over 30,000 biomolecules such as cholesterol, vitamin K, coenzyme Q10, and all steroid hormones.
Protein S (also known as PROS) is a vitamin K-dependent plasma glycoprotein synthesized in the liver. In the circulation, Protein S exists in two forms: a free form and a complex form bound to complement protein C4b-binding protein (C4BP). In humans, protein S is encoded by the PROS1 gene. [5] [6] Protein S plays a role in coagulation.
Vitamin K 1-deficiency may occur by disturbed intestinal uptake (such as would occur in a bile duct obstruction), by therapeutic or accidental intake of a vitamin K 1-antagonist such as warfarin, or, very rarely, by nutritional vitamin K 1 deficiency. As a result, Gla-residues are inadequately formed and the Gla-proteins are insufficiently active.
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Vitamin K deficiency from other causes (e.g., in malabsorption) or impaired vitamin K metabolism in disease (e.g., in liver failure) lead to the formation of PIVKAs (proteins formed in vitamin K absence), which are partially or totally non-gamma carboxylated, affecting the coagulation factors' ability to bind to phospholipid.