Abstract

Vitamin K is used as an anti-osteoporosis drug in Japan. Moreover, vitamin K intake has been found to decrease hip fracture risk. In the bone homeostasis, vitamin K action is mediated through two molecular mechanisms: posttranslational modification of proteins, and regulation of gene expression. The former is vitamin K-dependent carboxylation, in which vitamin K functions as an essential cofactor for modification of glutamic acid residues to gamma-carboxyglutamic acid residues. The latter is a novel mechanism that regulates the transcription of target genes by vitamin K through activation of steroid and xenobiotic receptor (SXR). The two mechanisms may coordinately contribute to vitamin K function in the bone metabolism.

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