VITAMIN-K STATUS INFLUENCES BRAIN SULFATIDE METABOLISM IN YOUNG MICE AND RATS

The established role of vitamin K in nutrition is as a cofactor in the post-translational conversion of specific glutamyl to gamma-carboxygl utamyl (Cia) residues in a limited number of proteins. Administration of the vitamin K antagonist warfarin has previously been shown to decr ease brain sulfatide concentrations and decrease brain galactocerebros ide sulfotransferase (GST) activity in young mice. A dietary deficienc y of vitamin K has now been shown to decrease (P < 0.01) brain sulfati de concentrations of 30-d-old mice significantly (by 21%). Male 21-d-o ld rats fed an excess of vitamin K for 7 or 14 d had 26 and 31% (P < 0 .05) greater GST activity and 15 and 18% (P < 0.05) greater brain sulf atide concentrations, respectively, than controls fed a vitamin K-defi cient diet. Male 21-d-old rats fed a diet containing 500 mg of phylloq uinone/kg diet had an intermediate response and were vitamin K suffici ent by normal criteria. The vitamin K response was observed when eithe r phylloquinone or menaquinone-4 was fed as a source of the vitamin. T hese data suggest that in addition to its recognized role in Gla synth esis, vitamin K status is important in the maintenance of normal compl ex lipid sulfatide metabolism in young rats and mice.