The parent structure of the vitamin K group is 2-methyl-1,4-napthoquinone, also known as menadione. Menadione is not a natural constituent of foods but does possess biological activity in vertebrates (Shearer, 2000). Constituents of the naturally occurring vitamin K group all possess the napthoquinone ring structure but differ in the structure of the side chain at the 3 position. There are two main groups according to whether plants or bacteria produce them. In plants, the major form of vitamin K is phylloquinone (vitamin K1), which has the same phytyl side chain as chlorophyll. Bacteria synthesise menaquinones (vitamin K2) with side chains based on a number of repeating prenyl units (MKn). The primary functions of vitamin K are in blood coagulation and in bone metabolism.
The major dietary sources of vitamin K are shown in Table 3.2; however, green vegetables contain the highest concentrations and are the largest contributors to dietary intakes (Booth et al, 1996). The relative phylloquinone content of vegetables reflects its association with photosynthetic tissues, with highest values being found in dark green leafy vegetables, e.g. spinach and cabbage (300600 mg/100g). Fermented cheeses contain two major menaquinones MK-8 and MK-9 at concentrations of 50-100 and 10-20 mg/100g respectively. Moulds do not normally synthesise menaquinones so MK-8 and 9 are thought to be derived from the starter fermentation bacteria.
Many bacteria present in the human intestine synthesise menaquinones, the major forms being MK-10 and -11 produced by Bacteroides, MK-8 by Enter-obacteria, MK-7 by Veillonella and MK-6 by Eubacterium lentum. Most are found in the distal colon where the menaquinone content is about 20 mg/100g dry weight, but there is no direct evidence that this pool is bioavailable. However, the widespread presence of very long-chain forms in the liver, e.g. MK10-13, does require explanation because these forms are not detected in commonly eaten foods but are typical of those produced by Bacteroides (Conly, 1992). There is, therefore, some debate as to the contribution of intestinal-derived K2 to vitamin K status (Lipsky, 1994; Suttie, 1995).
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