Makishima Makoto, Lu Timothy T, Xie Wen, Whitfield G Kerr, Domoto Hideharu, Evans Ronald M, Haussler Mark R, Mangelsdorf David J
Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.
Science. 2002 May 17;296(5571):1313-6. doi: 10.1126/science.1070477.
The vitamin D receptor (VDR) mediates the effects of the calcemic hormone 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. VDR is an order of magnitude more sensitive to LCA and its metabolites than are other nuclear receptors. Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. These studies offer a mechanism that may explain the proposed protective effects of vitamin D and its receptor against colon cancer.
维生素D受体(VDR)介导钙调节激素1α,25 - 二羟基维生素D3 [1,25(OH)2D3]的作用。我们发现,VDR还作为次级胆汁酸石胆酸(LCA)的受体发挥作用,LCA具有肝毒性且是一种潜在的肠道致癌物。VDR对LCA及其代谢产物的敏感性比其他核受体高一个数量级。LCA或维生素D激活VDR可在体内诱导CYP3A的表达,CYP3A是一种细胞色素P450酶,可在肝脏和肠道中使LCA解毒。这些研究提供了一种机制,可能解释维生素D及其受体对结肠癌的拟保护作用。