Exendin-4, a glucagon-like peptide-1 receptor agonist downregulates hepatic receptor for advanced glycation end products in non-alcoholic steatohepatitis rat model
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY • 2018
Publication Information
Authors
Mona M. Allam & Walaa B. El gazzar
Keywords
Exendin-4; high-fat diet;
non-alcoholic steatohepatitis;
receptor for advanced
glycation end products;
oxidative stress; obesity;
hormone; oxidative stress
Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Publisher
taylor and francis group
Volume
124
Issue
1
Pages
10-17
publication.type
International
Paper Link
Open Link
Supplementary Materials
Not Available
Abstract
Context: Exendin-4, a glucagon-like peptide-1 receptor agonist has been shown to have curative
effects on hepatic steatosis in murine models.
Objective: The present study aimed to elucidate the effect of Exendin-4 on hepatic receptor for
advanced glycation end products (RAGE) mRNA expression in non-alcoholic steatohepatitis (NASH) rat
model induced by high-fat diet.
Methods: NASH was induced by high-fat diet intake, and Exendin-4 was given in two different doses.
After 12 weeks, liver enzyme levels, hepatic triglycerides, antioxidant enzymes and malondialdehyde
(MDA) levels, and mRNA RAGE was detected using RT-PCR.
Results: Exendin-4 in high dose reduced significantly liver enzymes activity, hepatic triglycerides, MDA
levels and hepatic mRNA RAGE expression levels with significantly higher antioxidant enzymes activity.
Conclusions: Our results give further insights into the mechanisms underlying the curative role of
Exendin-4 in NASH, suggesting that interference with RAGE may be a useful therapeutic approach to
NASH.
effects on hepatic steatosis in murine models.
Objective: The present study aimed to elucidate the effect of Exendin-4 on hepatic receptor for
advanced glycation end products (RAGE) mRNA expression in non-alcoholic steatohepatitis (NASH) rat
model induced by high-fat diet.
Methods: NASH was induced by high-fat diet intake, and Exendin-4 was given in two different doses.
After 12 weeks, liver enzyme levels, hepatic triglycerides, antioxidant enzymes and malondialdehyde
(MDA) levels, and mRNA RAGE was detected using RT-PCR.
Results: Exendin-4 in high dose reduced significantly liver enzymes activity, hepatic triglycerides, MDA
levels and hepatic mRNA RAGE expression levels with significantly higher antioxidant enzymes activity.
Conclusions: Our results give further insights into the mechanisms underlying the curative role of
Exendin-4 in NASH, suggesting that interference with RAGE may be a useful therapeutic approach to
NASH.
Staff Members - Benha University