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PMID:14739254
| Citation |
Volle, DH, Repa, JJ, Mazur, A, Cummins, CL, Val, P, Henry-Berger, J, Caira, F, Veyssiere, G, Mangelsdorf, DJ and Lobaccaro, JM (2004) Regulation of the aldo-keto reductase gene akr1b7 by the nuclear oxysterol receptor LXRalpha (liver X receptor-alpha) in the mouse intestine: putative role of LXRs in lipid detoxification processes. Mol. Endocrinol. 18:888-98 |
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| Abstract |
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 by retinoic X receptor/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 LXRalpha 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. |
| Links |
PubMed Online version:10.1210/me.2003-0338 |
| Keywords |
Aldehyde Reductase/biosynthesis; Aldehyde Reductase/genetics; Animals; Binding Sites; DNA-Binding Proteins; Gene Expression Regulation/physiology; Intestines/metabolism; Lipid Metabolism; Lipids/toxicity; Mice; Mice, Knockout; Orphan Nuclear Receptors; Promoter Regions, Genetic; Receptors, Cytoplasmic and Nuclear/agonists; Receptors, Cytoplasmic and Nuclear/genetics; Receptors, Cytoplasmic and Nuclear/metabolism |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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