Vitamin K is a nutrient originally identified as an essential factor for blood coagulation. Recently,
vitamin K has emerged as a potential protector against
osteoporosis and hepatocarcinoma. Accumulated evidence indicates that subclinical non-
hemostatic vitamin K deficiency in extrahepatic tissues, particularly in bone, exists widely in the otherwise healthy adult population. Both
vitamin K(1) and K(2) have been shown to exert protective effects against
osteoporosis. Moreover, therapeutic potential of
vitamin K(2) as an anti-
hepatoma drug has been recently highlighted. Most of the new
biological functions of
vitamin K in bone and
hepatoma cells are considered to be attributable to promotion of gamma-carboxylation of
glutamic acid residues in
vitamin K-dependent
proteins, which is shared by both
vitamins K(1) and K(2). In contrast,
vitamin K(2)-specific, gamma-carboxylation-unrelated functions have also been demonstrated. These functions include stimulation of
steroid and xenobiotic receptor (SXR)-mediated transcription and
anti-oxidant property. Thus,
biological differences between
vitamins K(1) and K(2), and a potential involvement of gamma-carboxylation-independent actions in the new roles of
vitamin K remain open issues. Molecular bases of coagulation-unrelated pleiotropic actions of
vitamin K and its implications in human health deserve further investigations.