Effect of vitamin K on the calcium channel (TRPV6) and calbindin-D9k genes in the gastrointestinal tract of rats and Caco-2 cells.

最近，维生素K作为类固醇和异生素受体（SXR）的配体在成骨细胞中通过转录调控发挥作用的新机制被报道。TRPV 6、calbindin-D9 k和PMCA 1b基因参与了小肠粘膜细胞钙吸收过程，并被维生素D诱导表达。SXR在小肠中也有高水平表达，其结合位点含有维生素D受体（VDR）的结合基序。因此，我们推测维生素K可能与VDR结合基序结合，调控肠道钙吸收相关基因的表达。结肠癌细胞系SW-480揭示了通过添加维生素K2增加TRPV 6 mRNA表达。本研究通过给大鼠喂饲维生素K，分析TRPV 6和calbindin-D9 k mRNA表达的变化。维生素K饮食增加TRPV 6和钙结合蛋白-D9 k的表达。

Recently, a novel mechanism of vitamin K functions via transcriptional regulation as a ligand for steroid and xenobiotic receptor (SXR) in osteoblastic cells was reported. Three genes, TRPV6, calbindin-D9k and PMCA1b were determined to be involved in the process of calcium absorption in the mucosal cells of intestine and induced gene expression by vitamin D.SXR is also expressed at high level in intestine and SXR-binding site contains binding motifs for vitamin D receptor (VDR). Therefore we expected that vitamin K bound to VDR binding motif and regulated the expression of genes that were involved in calcium absorption in intestine. Colon cancer cell line SW-480 revealed the increase of the TRPV6 mRNA expression by the addition of vitamin K2. In this study, we fed rats vitamin K supplemented diet and analyzed the change of expression of TRPV6 and calbindin-D9k mRNA. The vitamin K diet increased expression of TRPV6 and calbindin-D9k.