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作为成骨细胞中类固醇和异种生物受体(SXR)的配体，通过转录调控发挥作用的新机制被报道。TRPV6、Calbindin-D9k和PMCA1b三个基因参与了肠粘膜细胞的钙吸收过程，并被维生素D诱导表达。SXR在肠道中也有高水平的表达，SXR结合部位含有维生素D受体(VDR)的结合基序。因此，我们推测维生素K与VDR结合基序结合，并调控与肠道钙吸收相关的基因表达。加入维生素K2后，结肠癌细胞株SW-480的TRPV6mRNA表达增加。本研究通过添加维生素K饲料喂养大鼠，分析其对TRPV6和Calbindin-D9k基因表达的影响。维生素K饮食增加了TRPV6和Calbindin-D9k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.