Vitamin K (Menaquinone-7, MK-7) - Nutrition

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What is Vitamin K (Menaquinone-7, MK-7)?

Vitamin K is category of essential fat-soluble vitamins that consist of napthaquinone rings with aliphatic side-chains. They are found naturally-occurring in the diet as one of two forms: plant-derived vitamin K1 (phylloquinone) or animal-derived vitamin K2 (menaquinone-7 or MK-7), the latter is derived from bacterial synthesis in the gastrointestinal tract. Vitamin K3 (menadione) is a synthetic compound, often used as a dietary supplement in animal feeds[1]. However this form of vitamin K (menadione) is not biologically active, until it is converted to vitamin K2 (MK-7) by intestinal microbes prior to absorption. Vitamin K is incorporated into mixed micelles along with dietary fat and absorbed by diffusion across the mucosal surface of the small intestine. Once in the enterocytes, absorbed vitamin K is incorporated into chylomicrons and released into the lymphatics for transport to the liver. Vitamin K is primarily excreted through bile in faeces, though significant amounts are also lost through urine.

Why is it Important?

Vitamin K is important for normal blood clotting and bone formation. Under normal circumstances endogenous production of vitamin K bacterial synthesis in the gastrointestinal tract is sufficient to meet metabolic requirements.

Roles in the Body

  1. Coagulation Factors: The aliphatic side-chain on MK-7 serves as a substrate for γ-glutamyl carboxylase, which results in carboxylation of glutamyl residues on prothrombin (i.e. factor II), as well as the glutamyl residues on coagulation factors VII, IX, X[2]. This carboxylation facilitates Ca2+ binding and activation of these proteins, which initiates the coagulation cascade[3]. Decarboxylated MK-7 forms a vitamin-K-epoxide that must be recycled through reaction with a vitamin-K-epoxide reductase in the liver.
  2. Bone Health: Osteocalcin is secreted by osteoblasts and is the second most abundant protein in bone[4]. Glutamyl residues on osteocalcin are carboxylated by vitamin-K-dependant carboxylase enzymes and allow Ca2+ binding and subsequent formation of hydroxyapatite in bone.

Consequences of Vitamin K Deficiency


Clinical signs of vitamin K deficiency include prolonged bleeding times that can progress to internal haemorrhage and death if not treated. Because of adequate microbial synthesis, naturally occurring vitamin K deficiencies have not been reported in dogs. Relative deficiencies can occur due to vitamin K antagonist exposure (i.e. warfarin toxicity)[5] or in animals with synthetic liver failure.


Clinical signs of vitamin K deficiency in kittens and adult cats include prolonged bleeding times, internal haemorrhage, and death. Congenital defects in γ-glutamyl carboxylase have been described in Devon Rex cats[6], and the feeding of fish-based diets does not support adequate microbial vitamin K synthesis[7] and can result in a vitamin K deficiency unless supplemental vitamin K is added to the diet. Relative deficiencies can occur in cats due to vitamin K antagonist exposure (i.e. warfarin toxicity) or in animals with chronic liver or intestinal disease[8].


There are no published reports of MK-7 and phylloquinone toxicity in dogs and cats and oral menadione has only been shown to be toxic when given at 1000x the requirement[1]. Conversely, parenteral menadione is toxic in all species and can cause haemolytic anaemia at low dosages and should not be given[1].

Dietary Sources

Vitamin K is found in varied concentrations in all foodstuffs. Liver has higher concentrations of MK-7 than other animal proteins such as muscle meat, dairy, and eggs. Phylloquinone is concentrated in the leaves of dark-green vegetables (e.g. spinach, kale, broccoli) as well as pulses (i.e. legumes), while cereal grains and other fruits and vegetables have lower concentrations of phylloquinone. Menadione is used as a vitamin K supplement in commercial dog and cat foods.

Diagnosing Vitamin K Deficiency

A true deficiency of Vitamin K is rarely encountered in clinical practice; a relative deficiency resulting from intoxication with a Vitamin K antagonist (e.g. Warfarin) is more likely. A clinical suspicion arises when animals have bleeding tendencies (e.g. haemorrhage) compatible clinical signs and prolongation of prothrombin time (PT) and possibly activated partial thromboplastin time (aPTT). Measuring elevated levels of Proteins Induced by Vitamin K Antagonism (PIVKA) is a sensitive indicator for vitamin K deficiency and enables confirmation of the diagnosis; however, PIVKA is not a direct vitamin K test but simply a more sensitive assay for PT[9].


  1. 1.0 1.1 1.2 National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.210-212.
  2. Suttie JW. Vitamin K. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.568-583.
  3. Winter RL, et al. Aortic thrombosis in dogs: presentation, therapy, and outcome in 26 cases. J Vet Cardiol 2012;14:333-342.
  4. Neve A, et al. Osteocalcin: skeletal and extra-skeletal effects. J Cell Physiol 2013;228:1149-1153.
  5. Clark WT and Halliwell REW. The treatment of vitamin K preparation of warfarin poisoning in dogs. Vet Rec 1963;75:1210-1213.
  6. Soute BA, et al. Congenital deficiency of all vitamin K-dependent blood coagulation factors due to a defective vitamin K-dependent carboxylase in Devon Rex cats. Thromb Haemost 1992;68:521-525.
  7. Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Pract 1996;37:322-326.
  8. Center SA, et al. Proteins invoked by vitamin K absence and clotting times in clinically ill cats. JVIM 2000 14:292-297.
  9. Mount ME, et al. Use of a test for proteins induced by vitamin K absence or antagonism in diagnosis of anticoagulant poisoning in dogs: 325 cases (1987-1997). JAVMA 2003;222:194-198.

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