Abstract
In the present study, we show that the expression of type 2 glucose transporter isoform (GLUT2) could be regulated by PPAR-γ in the liver. Rosiglitazone, PPAR-γ agonist, activated the GLUT2 mRNA level in the primary cultured hepatocytes and Alexander cells, when these cells were transfected with PPAR-γ/RXR-α. We have localized the peroxisome proliferator response element in the mouse GLUT2 promoter by serial deletion studies and site-directed mutagenesis. Chromatin immunoprecipitation assay using ob/ob mice also showed that PPAR-γ rather than PPAR-α binds to the -197/-184 region of GLUT2 promoter. Taken together, liver GLUT2 may be a direct target of PPAR-γ ligand contributing to glucose transport into liver in a condition when PAPR-γ expression is increased as in type 2 diabetes or in severe obesity.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Im, SS., Kim, JW., Kim, TH. et al. Identification and characterization of peroxisome proliferator response element in the mouse GLUT2 promoter. Exp Mol Med 37, 101–110 (2005). https://doi.org/10.1038/emm.2005.14
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DOI: https://doi.org/10.1038/emm.2005.14
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