Vitamin K requirement of mammals is met by a combination of dietary intake and microbial biosynthesis in the gut, which may involve intestinal microorganisms (such as Escherichia coli). Animals that practice some degree of coprophagy, such as the dog, can utilize much of the vitamin K that is eliminated in the feces. In rats, the majority of menaquinone absorbed resulted from fecal ingestion compared to dietary sources or from direct synthesis and absorption from the intestine (Kindberg et al., 1987). Duello and Matschiner (1971a, b) isolated 19 vitamin K analogs in dog liver and suggested that most were absorbed from the intestine, all of which were presumably derived from bacterial synthesis in the intestine.
Animal feces contain substantial amounts of vitamin K even when none is present in feed. Despite the intestinal synthesis, animals can be rendered deficient when fed vitamin K-free diets, and coprophagy is prevented if animals are maintained germ-free or if a vitamin K antagonist is given. Difficulties in demonstrating dietary requirement in many species include the varying degrees to which they utilize vitamin K synthesized by intestinal bacteria and the degree to which different species practice coprophagy.
Vitamin K requirements can be altered by age, sex, breed, antivitamin K factors, disease conditions and any condition influencing lipid absorption or altering intestinal flora. Rapid rate of food passage through the digestive tract may also influence vitamin K synthesis in the pig. Swine are able to obtain more benefit from vitamin K intestinal synthesis than are poultry. First defecation in pigs, for a specific portion of diet, may occur about 15 hours after feeding, but most of the given meal will be retained in the tract appreciably longer. A comparable time period for chickens would be approximately three hours (Griminger, 1984) and consequently, less vitamin K synthesis and absorption occur. For dogs and cats, a slower rate of food passage, more similar to the pig vs. the chicken, would be expected.
Excess vitamin A and calcium has been shown to influence vitamin K requirements. Rats fed excess retinol had two- to threefold higher carboxylase activities of endogenous, prothrombin precursors, which is an indicator of vitamin K deficiency. Hall et al. (1991) reported a hemorrhagic condition in pigs fed 2.7% dietary calcium. The condition was cured with vitamin K supplementation and was not produced in treatments receiving less dietary calcium.
Neither vitamin K absorption, function nor requirement has been studied in cats. Requirements for vitamin K for both dogs and cats are low compared to other species. Although no evidence of vitamin K deficiency was observed in dogs or cats fed a diet containing 60 µg of vitamin K activity per kg (27.3 µg per lb), 75% of rats fed this diet died of hemorrhage (Reber and Malhotra, 1961).