Menaquinone-7 regulates the expressions of osteocalcin, OPG, RANKL and RANK in osteoblastic MC3T3E1 cells

Effect of vitamin K2 on progression of atherosclerosis and vascular calcification in nondialyzed patients with chronic kidney disease stages 3–5

“…26 In our study, the serum OPG increased during supplementation with vitamin K 2 . Our findings confirm the previous experimental 27 and human studies 28 measured before and after the treatment; however, the patient's compliance may be confirmed by the change of dp-ucMGP and 25(OH)D levels observed in both groups. In addition, we did not notice any significant differences between the treated groups over time; we only found differences within the groups and between the groups at baseline and at final measurement.…”

Vitamin K2 stimulates osteoblastogenesis and suppresses osteoclastogenesis by suppressing NF-κB activation

“…Vitamin K2 has been reported to directly stimulate RANKL expression by MC3T3 osteoblastic cells (50). This may be a consequence of the capacity of vitamin K2 to promote osteoblast differentiation as observed in our study.…”

Vitamin K2 supplementation does not influence bone loss in early menopausal women: a randomised double-blind placebo-controlled trial

“…Vitamin K promotes post-translational conversion of protein glutamate residues in osteocalcin into gamma-carboxy glutamate (Gla) [11,12], which is secreted by the osteoblasts. Vitamin K deficiency will cause production of under-carboxylated osteocalcin (ucOC) [13], and ucOC levels are therefore considered to be a sensitive measure of vitamin K status [14].…”

“…Both vitamin K1 (phylloquinone or phytonadione) and K2 (menaquinone) contribute to the vitamin K status in humans [12] (Table 1). Vitamin K2 is a spectrum of multiple forms where menaquinone-4 (MK-4) and menaquinone-7 (MK-7) are reportedly related to bone mass and fracture risk [11,12]. A systematic review from 2006 indicated that supplementation with phytonadione and MK-4 may reduce bone loss and fracture risk [17].…”