Vitamin K Biochemistry
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Vitamins
- Vitamin B1 (Thiamine) Biochemistry
- Vitamin B1 (Thiamine) Deficiency
- Vitamin B2 (Riboflavin)
- Vitamin B3 (Niacin) Biochemistry
- Vitamin B3 (Niacin) Deficiency and Excess
- Hartnup Disease
- Vitamin B5 (Pantothenic Acid)
- Vitamin B6 (Pyridoxine)
- Vitamin B7 (Biotin)
- Vitamin B9 (Folate)
- Vitamin B12 (Cobalamin) Biochemistry
- Vitamins B9 and B12 Deficiencies
- Vitamin A (Retinol) Biochemistry
- Vitamin A (Retinol) Deficiency and Excess
- Vitamin C (Ascorbic Acid) Biochemistry
- Vitamin C (Ascorbic Acid) Deficiency and Excess
- Vitamin D Biochemistry
- Vitamin D Deficiency and Excess
- Vitamin E (Tocopherol/Tocotrienol)
- Vitamin K Biochemistry
- Vitamin K Deficiency
- Zinc
- Kwashiorkor and Marasmus
Summary
Vitamin K is a fat-soluble vitamin synthesized by intestinal bacteria. Vitamin K is activated by the enzyme epoxide reductase to its reduced form, which acts as a cofactor for gamma-carboxylation of glutamic acid residues on blood clotting proteins. Therefore, Vitamin K plays an important role in coagulation (formation of blood clots), as there are a number of such vitamin K-dependent coagulation factors: including factors II, VII, IX, X, as well as protein C and S.
Key Points
- Vitamin K
- Fat-soluble compounds synthesized by intestinal flora
- Includes phytomenadione, phylloquinone, phytonadione
- Vitamin K Deficiency typically caused by fat malabsorption
- Activated by epoxide reductase to reduced form
- Active Vitamin K is a cofactor for the y-carboxylation of glutamic acid residues needed to synthesize blood clotting factors
- Vitamin K-dependent proteins include Factors II, VII, IX, X, proteins C and S
- Warfarin (Coumadin) inhibits epoxide reductase, blocking vitamin K-mediated gamma-carboxylation
- Active Vitamin K is a cofactor for the y-carboxylation of glutamic acid residues needed to synthesize blood clotting factors
- Fat-soluble compounds synthesized by intestinal flora
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