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Vitamin K Status Influences Brain Sulfatide Metabolism in Young Mice and Rats1,2,

K. S. Sundaram, J.-H. Fan, J. A. Engelke*, A. L. Foley*, J. W. Suttie* and M. Lev3

Department of Microbiology and Immunology, CUNY Medical School, City College, New York, NY 10031 * Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, Madison, WI 53706

The established role of vitamin K in nutrition is as a cofactor in the post-translational conversion of specific glutamyl to {gamma}-carboxyglutamyl (Gla) residues in a limited number of proteins. Administration of the vitamin K antagonist warfarin has previously been shown to decrease brain sulfatide concentrations and decrease brain galactocerebroside sulfotransferase (GST) activity in young mice. A dietary deficiency of vitamin K has now been shown to decrease (P < 0.01) brain sulfatide concentrations of 30-d-old mice significantly (by 21%). Male 21-d-old 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 sulfatide concentrations, respectively, than controls fed a vitamin K-deficient diet. Male 21-d-old rats fed a diet containing 500 mg of phylloquinone/kg diet had an intermediate response and were vitamin K sufficient by normal criteria. The vitamin K response was observed when either phylloquinone or menaquinone-4 was fed as a source of the vitamin. These data suggest that in addition to its recognized role in Gla synthesis, vitamin K status is important in the maintenance of normal complex lipid sulfatide metabolism in young rats and mice.


KEY WORDS: • vitamin K • brain sulfatides • galactocerebroside sulfotransferase • warfarin • rats • mice

1 Supported by the Research Center for Minority Institutions Grant RR03060, a PSC-CUNY award, a grant from the Thompson Medical Foundation, and by the College of Agricultural and Life Sciences of the University of Wisconsin-Madison, and program project grant DK14881 from the National Institutes of Health, Bethesda, Maryland.

2 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

3 To whom correspondence should be addressed.

Manuscript received 20 February 1996. Revision accepted 31 July 1996.







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