Kvitaminban

Kvitaminban, in biochemistry and nutrition, refers to the cellular and enzymatic pathway by which vitamin K participates in the carboxylation of glutamate residues in certain proteins. The family of vitamin K compounds includes phylloquinone (vitamin K1) and various menaquinones (vitamin K2). In the pathway, vitamin K is present in the reduced hydroquinone form, which acts as a cofactor for the enzyme gamma-glutamyl carboxylase. The enzyme carboxylates specific glutamate residues in vitamin K-dependent proteins, converting them to gamma-carboxyglutamate, enabling calcium binding and biological activity. After this reaction, vitamin K is oxidized to vitamin K epoxide and must be recycled back to its active form. The recycling is mediated primarily by the vitamin K epoxide reductase (VKOR) system, which regenerates the hydroquinone from the epoxide. The cycle thus maintains a supply of active vitamin K for continuous protein carboxylation. The process is essential for the function of coagulation factors II, VII, IX, and X, as well as anticoagulant proteins C and S, and it also regulates extrahepatic proteins such as osteocalcin and matrix Gla protein involved in bone and vascular biology.

Dietary vitamin K is absorbed with fats and transported in lipoproteins; liver primarily stores K1, while tissues outside the liver accumulate K2 forms. Warfarin and related anticoagulants inhibit VKOR, reducing recycling and thereby impairing gamma-carboxylation. Clinically, Kvitaminban is discussed in contexts of blood coagulation, osteoporosis risk, and drug-nutrient interactions. In healthy individuals with normal gut function, a balanced diet typically maintains adequate vitamin K status.