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We wished to investigate the mechanism of decreased serum vitamin K1 after bone fractures. Vitamin K1 plays a role in bone formation because it is required as a cofactor for the transformation of glutamic acid (Glu) residues on proteins to γ-carboxyglutamic acid (Gla) residues. The double carboxy group on Gla residues has high affinity for the binding of calcium. Bone formation involves vitamin K-dependent small peptide osteocalcin (bone-Gla-protein) that is secreted by osteoblasts.Serum concentrations of vitamin K1 reflect in part the capacity of the serum to carry the vitamin. Vitamin K1 is a lipid, and little is known about the binding of this vitamin to proteins other than that it is transported in serum by the lipoproteins. It is not known whether there is a specific “vitamin K1-binding protein” in tissues as has been suggested for vitamin E as a “tocopherol-binding protein” (1).Deficiency of vitamin K will lead to defective γ-carboxylation of vitamin K-dependent proteins and will be manifested by the failure of these proteins to function normally (2)(3)(4)(5)(6)(7)(8). Low serum concentrations of vitamin K1 have been reported to occur in patients with traumatic bone fractures (4)(5)(6), although others have reported nonsignificant decreases in vitamin K1 in the immediate 48 h after low-energy trauma hip fracture (9). These serum concentrations were considered pathological because they were significantly lower than values in age-matched control subjects. Recent studies, however, have shown that even very low absolute concentrations of vitamin K1 in serum do not reflect the vitamin K status (3)(10)(11). The use of a relative measure of serum vitamin K1, the ratio of vitamin …

What Happens to Vitamin K1 in Serum after Bone Fracture?