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

Exp Mol Med. 2005 Apr 30;37(2):101-10. doi: 10.1038/emm.2005.14.

Abstract

In the present study, we show that the expression of type 2 glucose transporter isoform (GLUT2) could be regulated by PPAR-gamma in the liver. Rosiglitazone, PPAR-gamma agonist, activated the GLUT2 mRNA level in the primary cultured hepatocytes and Alexander cells, when these cells were transfected with PPAR-gamma/RXR-alpha. 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-gamma rather than PPAR-alpha binds to the -197/-184 region of GLUT2 promoter. Taken together, liver GLUT2 may be a direct target of PPAR-gamma ligand contributing to glucose transport into liver in a condition when PAPR-gamma expression is increased as in type 2 diabetes or in severe obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Chromatin Immunoprecipitation
  • Gene Expression Regulation
  • Genes, Reporter
  • Glucose Transporter Type 2
  • Hepatocytes / metabolism*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred ICR
  • Mice, Transgenic
  • Monosaccharide Transport Proteins / biosynthesis*
  • Monosaccharide Transport Proteins / genetics
  • Mutagenesis, Site-Directed
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • PPAR gamma / agonists
  • PPAR gamma / genetics
  • PPAR gamma / metabolism*
  • Promoter Regions, Genetic*
  • Protein Isoforms / biosynthesis
  • Response Elements*
  • Rosiglitazone
  • Thiazolidinediones / pharmacology

Substances

  • Glucose Transporter Type 2
  • Monosaccharide Transport Proteins
  • PPAR alpha
  • PPAR gamma
  • Protein Isoforms
  • Thiazolidinediones
  • Rosiglitazone