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Submitted on September 4, 2003
Accepted on January 14, 2004
in the Mouse Intestine: Putative Role of LXRs in Lipid Detoxification Processes
Physiologie Comparée et Endocrinologie Moléculaire, UMR CNRS 6547, Aubière, France (D.H.V., P.V., J.H.-B., F.C., G.V., J.-M.A.L.); Department of Pharmacology and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas (J.J.R., C.L.C., D.J.M.); Unité Maladies Métaboliques et Micronutriments, INRA, Saint-Genès-Champanelle, France (A.M.).
* To whom correspondence should be addressed. E-mail: j-marc.lobaccaro{at}geem.univ-bpclermont.fr.
Liver X receptors (LXRs) regulate the expression of a number of genes involved in cholesterol and lipid metabolism after activation by their cognate oxysterol ligands. AKR1-B7 (aldo-keto reductase 1-B7) is expressed in LXR target tissues such as intestine, and because of its known role in detoxifying lipid peroxides, we investigated whether the AKR1-B7 detoxification pathway was regulated by LXRs. Here we show that synthetic LXR agonists increase the accumulation of AKR1-B7 mRNA and protein levels in mouse intestine in wild-type but not lxr-/- mice. Regulation of akr1b7 byRXR/LXR heterodimers is dependent on three response elements in the proximal murine akr1b7 promoter. Two of these cis-acting elements are specific for regulation by the LXR
isoform. In addition, in duodenum of wild-type mice fed a synthetic LXR agonist, we observed an LXR-dependent decrease in lipid peroxidation. Our results demonstrate that akr1b7 is a direct target of LXRs throughout the small intestine, and that LXR activation plays a protective role by decreasing the deleterious effects of lipid peroxides in duodenum. Taken together, these data suggest a new role for LXRs in lipid detoxification.
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