Identification and characterization of peroxisome proliferator response element in the mouse GLUT2 promoter

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.