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© 2008 American Society for Nutrition J. Nutr. 138:492-496, March 2008


Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Age and Dietary Form of Vitamin K Affect Menaquinone-4 Concentrations in Male Fischer 344 Rats1–3,

Sarah L. Booth*, James W. Peterson, Donald Smith, M. Kyla Shea, John Chamberland and Natalia Crivello

Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111

* To whom correspondence should be addressed. E-mail: sarah.booth{at}tufts.edu.

Phylloquinone, the primary dietary form of vitamin K, is converted to menaquinone-4 (MK-4) in certain tissues. MK-4 may have tissue-specific roles independent of those traditionally identified with vitamin K. Fischer 344 male rats of different ages (2, 12, and 24 mo, n = 20 per age group) were used to compare the conversion of phylloquinone to MK-4 with an equivalent dose of another dietary form of vitamin K, 2',3'-dihydrophylloquinone. Rats were age- and diet-group pair-fed phylloquinone (198 ± 9.0 µg/kg diet) or dihydrophylloquinone (172 ± 13.0 µg/kg diet) for 28 d. MK-4 was the primary form of vitamin K in serum, spleen, kidney, testes, bone marrow, and brain myelin fractions, regardless of age group. MK-4 concentrations were significantly lower in kidney, heart, testes, cortex (myelin), and striatum (myelin) in the dihydrophylloquinone diet group compared with the phylloquinone diet group (P < 0.05). The MK-4 concentrations in 2-mo-old rats were lower in liver, spleen, kidney, heart, and cortex (myelin) but higher in testes compared with 24-mo-old rats (P < 0.05). However, there were no age-specific differences in MK-4 concentrations among the rats fed the 2 diets. These data suggest that dihydrophylloquinone, which differs from phylloquinone in its side phytyl chain, is absorbed but its intake results in less MK-4 in certain tissues. Dihydrophylloquinone may be used in models for the study of tissue-specific vitamin K deficiency.





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9-Cis Retinoic Acid Reduces 1{alpha},25-Dihydroxycholecalciferol-Induced Renal Calcification by Altering Vitamin K-Dependent {gamma}-Carboxylation of Matrix {gamma}-Carboxyglutamic Acid Protein in A/J Male Mice
J. Nutr., December 1, 2008; 138(12): 2337 - 2341.
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