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Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111
3To whom correspondence should be addressed. E-mail: sarah.booth{at}tufts.edu.
Biological markers indicative of poor vitamin K status have been associated with a greater risk for hip fracture in older men and women. However, the dietary phylloquinone intake required to achieve maximal carboxylation of hepatic and extrahepatic vitamin Kdependent proteins is not known. In an 84-d study in a metabolic unit, 21 older (6080 y) women were fed a phylloquinone-restricted diet (18 µg/d) for 28 d, followed by stepwise repletion of 86, 200 and 450 µg/d of phylloquinone. Plasma phylloquinone, urinary
-carboxyglutamic acid excretion and
-carboxylation of hepatic (prothrombin) and extrahepatic proteins (osteocalcin) decreased in response to phylloquinone restriction (P < 0.001), demonstrating the production of subclinical vitamin K deficiency. The
-carboxylation of prothrombin was restored to normal levels in response to phylloquinone supplementation at 200 µg/d. In contrast, all other biochemical markers of vitamin K status remained below normal levels after short-term supplementation of up to 450 µg/d of phylloquinone. These data support previous observations in rats that hepatic vitamin Kdependent proteins have preferential utilization of phylloquinone in response to phylloquinone dietary restriction. Moreover, our findings suggest that the current recommended Adequate Intake levels of vitamin K (90 µg/d) in women do not support maximal osteocalcin
-carboxylation in older women.
KEY WORDS: vitamin K deficiency undercarboxylated prothrombin undercarboxylated osteocalcin urinary
-carboxyglutamic acid adequate intake
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