ABSTRACT

This chapter highlights the sources, metabolism, and functions of vitamins. The catabolism of vitamin K1 in the intestine can generate vitamin K3, whereas the metabolism of vitamin K3 in animals can lead to vitamin K2. Through the metabolism of lipoproteins in the blood, vitamin K-rich chylomicrons are converted into chylomicron remnants, which are taken up by the liver through receptor-mediated mechanisms. In animals, a long-chain vitamin K2 is the major constituent of the hepatic vitamin K pool, with vitamin K1 being a minor one. Hemorrhagic disease can occur in newborn infants, who are particularly vulnerable to vitamin K deficiency. Animals fed nutrient-balanced diets do not exhibit abnormal metabolism or physiology when they do not consume dietary bioflavonoids. There is no evidence for nutritional roles of these substances in mammals, birds, or fish. Animals fed nutrient-balanced diets do not exhibit abnormal metabolism or physiology when they do not consume dietary para-aminobenzoic acid.