ChREBP regulates Pdx-1 and other glucose-sensitive genes in pancreatic β-cells

Research output: Contribution to journalArticlepeer-review

Authors

Colleges, School and Institutes

Abstract

Carbohydrate responsive element-binding protein (ChREBP) is a transcription factor whose expression and activity are increased in pancreatic β-cells maintained at elevated glucose concentrations. We show here that ChREBP inactivation in clonal pancreatic MIN6 β-cells results in an increase in Pdx-1 expression at low glucose and to a small, but significant, increase in Ins2, GcK and MafA gene expression at high glucose concentrations. Conversely, adenovirus-mediated over-expression of ChREBP in mouse pancreatic islets results in decreases in Pdx-1, MafA, Ins1, Ins2 and GcK mRNA levels. These data suggest that strategies to reduce ChREBP activity might protect against β-cell dysfunction in type 2 diabetes.

Details

Original languageEnglish
Pages (from-to)252-257
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume402
Issue number2
Publication statusPublished - 12 Nov 2010

Keywords

  • Animals, Base Sequence, Cell Line, Tumor, Gene Expression Regulation, Gene Silencing, Glucose/metabolism, Homeodomain Proteins/genetics, Insulin-Secreting Cells/drug effects, Mice, Molecular Sequence Data, Nuclear Proteins/genetics, Trans-Activators/genetics, Transcription Factors/genetics