Vitamin D Receptor As an Intestinal Bile Acid Sensor-Reference-Cited by-同舟云学术

Vitamin D Receptor As an Intestinal Bile Acid Sensor

Published:2002-05-17 Issue:5571 Volume:296 Page:1313-1316
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Makishima Makoto¹,Lu Timothy T.¹,Xie Wen²,Whitfield G. Kerr³,Domoto Hideharu¹,Evans Ronald M.²,Haussler Mark R.³,Mangelsdorf David J.¹

Affiliation:

1. Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390–9050, USA.

2. Howard Hughes Medical Institute, Gene Expression Laboratory, The Salk Institute for Biological Studies, Post Office Box 85800, San Diego, CA 92186–5800, USA.

3. Department of Biochemistry and Molecular Biophysics, College of Medicine, University of Arizona, Tucson, AZ 85724, USA.

Abstract

The vitamin D receptor (VDR) mediates the effects of the calcemic hormone 1α,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ]. 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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