Exp Mol Med.  2005 Apr;37(2):101-110.

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

Affiliations
  • 1Department of Biochemistry and Molecular Biology, Korea. yha111@yumc.yonsei.ac.kr
  • 2Center for Chronic Metabolic Disease Research, Korea.
  • 3Institute of Genetic Science, Korea.
  • 4Brain Korea 21 Project for Medical Science, Korea.
  • 5Yonsei University College of Medicine, 134 Sinchon-dong, Seodaemun-gu, Seoul, Korea.

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.

Keyword

GLUT2; liver; promoter; PPAR-gamma; rosiglitazone; type 2 diabetes
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