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

Gabriela da Silva Xavier; Gao Sun; Qingwen Qian; Guy A Rutter; Isabelle Leclerc

doi:10.1016/j.bbrc.2010.10.010

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

Gabriela da Silva Xavier, Gao Sun, Qingwen Qian, Guy A Rutter, Isabelle Leclerc

Metabolism and Systems Research

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

162 Downloads (Pure)

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.

Original language	English
Pages (from-to)	252-257
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	402
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2010.10.010
Publication status	Published - 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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Gabriela_da_Silva_Xavier_ChREBP_regulates_Pdx-1_and_othervglucose-sensitive_Biochemical_and_Biophysical_Research_Communications_2010
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Cite this

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title = "ChREBP regulates Pdx-1 and other glucose-sensitive genes in pancreatic β-cells",

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.",

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",

author = "{da Silva Xavier}, Gabriela and Gao Sun and Qingwen Qian and Rutter, {Guy A} and Isabelle Leclerc",

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doi = "10.1016/j.bbrc.2010.10.010",

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TY - JOUR

T1 - ChREBP regulates Pdx-1 and other glucose-sensitive genes in pancreatic β-cells

AU - da Silva Xavier, Gabriela

AU - Sun, Gao

AU - Qian, Qingwen

AU - Rutter, Guy A

AU - Leclerc, Isabelle

PY - 2010/11/12

Y1 - 2010/11/12

N2 - 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.

AB - 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.

KW - Animals

KW - Base Sequence

KW - Cell Line, Tumor

KW - Gene Expression Regulation

KW - Gene Silencing

KW - Glucose/metabolism

KW - Homeodomain Proteins/genetics

KW - Insulin-Secreting Cells/drug effects

KW - Mice

KW - Molecular Sequence Data

KW - Nuclear Proteins/genetics

KW - Trans-Activators/genetics

KW - Transcription Factors/genetics

U2 - 10.1016/j.bbrc.2010.10.010

DO - 10.1016/j.bbrc.2010.10.010

M3 - Article

C2 - 20934404

SN - 0006-291X

VL - 402

SP - 252

EP - 257

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 2

ER -

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

Abstract

Keywords

UN SDGs

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