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Dipeptedyl peptidase-4 (DPP-4) inhibitor downregulates HMGB1/TLR4/NF-ҡB signaling pathway in a diabetic rat model of non-alcoholic fatty liver disease
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY • 2021
Publication Information
Authors
Mona M. Allam, Reham M. Ibrahim, Walaa Bayoumie El Gazzar & Mona A.
Said
Keywords
Steatohepatitis; toll-like
receptor 4; sitagliptin; highmobility
group box 1
protein; nuclear factor-jB
Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Publisher
Taylor & Francis Group
Volume
Not Available
Issue
Not Available
Pages
Not Available
publication.type
International
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
Context: Inflammatory and immune pathways play a crucial role in the pathophysiology of non-alcoholic
fatty liver disease (NAFLD). Sitagliptin blocks the dipeptidyl peptidase-4 (DPP-4) enzyme, mechanisms
that alter inflammatory pathways and the innate immune system, and by which Sitagliptin
affects the pathogenesis of NAFLD weren’t previously discussed.
Objective: This study aims to understand the interaction between Sitagliptin and innate immune
response in order to meliorate NAFLD.
Methods: Thirty- two Wistar male albino rats were categorised into four groups. Rats have received a
standard diet or a high-fat diet either with or without Sitagliptin. Serum HMGB1, protein and mRNA
expressions of hepatic TLR4 and NF-jB, inflammatory cytokines, and histopathological changes
were analysed.
Results: An ameliorative action of Sitagliptin in NAFLD was demonstrated via decreasing HMGB1-
mediated TLR4/NF-jB signalling in order to suppress inflammation and reduce insulin resistance.
Conclusion: Sitagliptin may in fact prove to be a beneficial therapeutic intervention in NAFLD.
fatty liver disease (NAFLD). Sitagliptin blocks the dipeptidyl peptidase-4 (DPP-4) enzyme, mechanisms
that alter inflammatory pathways and the innate immune system, and by which Sitagliptin
affects the pathogenesis of NAFLD weren’t previously discussed.
Objective: This study aims to understand the interaction between Sitagliptin and innate immune
response in order to meliorate NAFLD.
Methods: Thirty- two Wistar male albino rats were categorised into four groups. Rats have received a
standard diet or a high-fat diet either with or without Sitagliptin. Serum HMGB1, protein and mRNA
expressions of hepatic TLR4 and NF-jB, inflammatory cytokines, and histopathological changes
were analysed.
Results: An ameliorative action of Sitagliptin in NAFLD was demonstrated via decreasing HMGB1-
mediated TLR4/NF-jB signalling in order to suppress inflammation and reduce insulin resistance.
Conclusion: Sitagliptin may in fact prove to be a beneficial therapeutic intervention in NAFLD.