Identification and characterization of peroxisome proliferator response element in the mouse GLUT2 promoter.
- Author:
Seung Soon IM
1
;
Jae Woo KIM
;
Tae Hyun KIM
;
Xian Li SONG
;
So Youn KIM
;
Ha Il KIM
;
Yong Ho AHN
Author Information
1. Department of Biochemistry and Molecular Biology, Korea. yha111@yumc.yonsei.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
GLUT2;
liver;
promoter;
PPAR-gamma;
rosiglitazone;
type 2 diabetes
- MeSH:
Animals;
Cells, Cultured;
Chromatin Immunoprecipitation;
Gene Expression Regulation;
Genes, Reporter;
Hepatocytes/*metabolism;
Liver/metabolism;
Male;
Mice;
Mice, Inbred ICR;
Mice, Transgenic;
Monosaccharide Transport Proteins/*biosynthesis/genetics;
Mutagenesis, Site-Directed;
PPAR alpha/genetics/metabolism;
PPAR gamma/agonists/genetics/*metabolism;
*Promoter Regions (Genetics);
Protein Isoforms/biosynthesis;
Research Support, Non-U.S. Gov't;
*Response Elements;
Thiazolidinediones/pharmacology
- From:Experimental & Molecular Medicine
2005;37(2):101-110
- CountryRepublic of Korea
- Language:English
-
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.
