Sundaram K S, Fan J H, Engelke J A, Foley A L, Suttie J W, Lev M
Department of Microbiology and Immunology, CUNY Medical School, City College, New York, NY 10031, USA.
J Nutr. 1996 Nov;126(11):2746-51. doi: 10.1093/jn/126.11.2746.
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.
维生素K在营养方面已确定的作用是作为一种辅助因子，参与有限数量蛋白质中特定谷氨酰基向γ-羧基谷氨酰基（Gla）残基的翻译后转化。先前的研究表明，给予维生素K拮抗剂华法林可降低幼鼠脑硫脂浓度，并降低脑半乳糖脑苷脂磺基转移酶（GST）活性。现已证明，饮食中维生素K缺乏会显著降低（P < 0.01）30日龄小鼠的脑硫脂浓度（降低21%）。雄性21日龄大鼠连续7天或14天摄入过量维生素K后，其GST活性分别比喂食维生素K缺乏饮食的对照组高26%和31%（P < 0.05），脑硫脂浓度分别高15%和18%（P < 0.05）。雄性21日龄大鼠喂食含500 mg叶绿醌/ kg饮食时，有中等反应，按正常标准维生素K充足。当以叶绿醌或甲萘醌-4作为维生素来源喂食时，均可观察到维生素K反应。这些数据表明，除了其在Gla合成中公认的作用外，维生素K状态对维持幼鼠正常的复合脂质硫脂代谢也很重要。
