Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway

<p dir="ltr">Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease worldwide. Agonists of the glucagon-like peptide-1 receptor (GLP-1R), currently approved to treat type 2 diabetes, hold promise to improve steatosis and even steatohepatitis. However, due to t...

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Main Author: Olfa Khalifa (10914452) (author)
Other Authors: Neyla S. AL-Akl (17886050) (author), Khaoula Errafii (10914446) (author), Abdelilah Arredouani (10914455) (author)
Published: 2022
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_version_ 1864513528355880960
author Olfa Khalifa (10914452)
author2 Neyla S. AL-Akl (17886050)
Khaoula Errafii (10914446)
Abdelilah Arredouani (10914455)
author2_role author
author
author
author_facet Olfa Khalifa (10914452)
Neyla S. AL-Akl (17886050)
Khaoula Errafii (10914446)
Abdelilah Arredouani (10914455)
author_role author
dc.creator.none.fl_str_mv Olfa Khalifa (10914452)
Neyla S. AL-Akl (17886050)
Khaoula Errafii (10914446)
Abdelilah Arredouani (10914455)
dc.date.none.fl_str_mv 2022-02-09T03:00:00Z
dc.identifier.none.fl_str_mv 10.1038/s41598-022-06143-5
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Exendin-4_alleviates_steatosis_in_an_in_vitro_cell_model_by_lowering_FABP1_and_FOXA1_expression_via_the_Wnt_-catenin_signaling_pathway/25125068
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Clinical sciences
Non-alcoholic fatty liver disease (NAFLD)
liver disease
diabetes
dc.title.none.fl_str_mv Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease worldwide. Agonists of the glucagon-like peptide-1 receptor (GLP-1R), currently approved to treat type 2 diabetes, hold promise to improve steatosis and even steatohepatitis. However, due to their pleiotropic effects, the mechanisms underlying their protective effect on NAFLD remain elusive. We aimed to investigate these mechanisms using an in vitro model of steatosis treated with the GLP-1R agonist Exendin-4 (Ex-4). We established steatotic HepG2 cells by incubating the cells with 400 µM oleic acid (OA) overnight. Further treatment with 200 nM Ex-4 for 3 h significantly reduced the OA-induced lipid accumulation (p < 0.05). Concomitantly, Ex-4 substantially reduced the expression levels of Fatty Acid-Binding Protein 1 (FABP1) and its primary activator, Forkhead box protein A1 (FOXA1). Interestingly, the silencing of β-catenin with siRNA abolished the effect of Ex-4 on these genes, suggesting dependency on the Wnt/β-catenin pathway. Additionally, after β-catenin silencing, OA treatment significantly increased the expression of nuclear transcription factors SREBP-1 and TCF4, whereas Ex-4 significantly decreased this upregulation. Our findings suggest that direct activation of GLP-1R by Ex-4 reduces OA-induced steatosis in HepG2 cells by reducing fatty acid uptake and transport via FABP1 downregulation.</p><h2>Other Information</h2><p dir="ltr">Published in: Scientific Reports<br>License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1038/s41598-022-06143-5" target="_blank">https://dx.doi.org/10.1038/s41598-022-06143-5</a></p>
eu_rights_str_mv openAccess
id Manara2_496aae119b47b89d6a809812d3a9114d
identifier_str_mv 10.1038/s41598-022-06143-5
network_acronym_str Manara2
network_name_str Manara2
oai_identifier_str oai:figshare.com:article/25125068
publishDate 2022
repository.mail.fl_str_mv
repository.name.fl_str_mv
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rights_invalid_str_mv CC BY 4.0
spelling Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathwayOlfa Khalifa (10914452)Neyla S. AL-Akl (17886050)Khaoula Errafii (10914446)Abdelilah Arredouani (10914455)Biomedical and clinical sciencesClinical sciencesNon-alcoholic fatty liver disease (NAFLD)liver diseasediabetes<p dir="ltr">Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease worldwide. Agonists of the glucagon-like peptide-1 receptor (GLP-1R), currently approved to treat type 2 diabetes, hold promise to improve steatosis and even steatohepatitis. However, due to their pleiotropic effects, the mechanisms underlying their protective effect on NAFLD remain elusive. We aimed to investigate these mechanisms using an in vitro model of steatosis treated with the GLP-1R agonist Exendin-4 (Ex-4). We established steatotic HepG2 cells by incubating the cells with 400 µM oleic acid (OA) overnight. Further treatment with 200 nM Ex-4 for 3 h significantly reduced the OA-induced lipid accumulation (p < 0.05). Concomitantly, Ex-4 substantially reduced the expression levels of Fatty Acid-Binding Protein 1 (FABP1) and its primary activator, Forkhead box protein A1 (FOXA1). Interestingly, the silencing of β-catenin with siRNA abolished the effect of Ex-4 on these genes, suggesting dependency on the Wnt/β-catenin pathway. Additionally, after β-catenin silencing, OA treatment significantly increased the expression of nuclear transcription factors SREBP-1 and TCF4, whereas Ex-4 significantly decreased this upregulation. Our findings suggest that direct activation of GLP-1R by Ex-4 reduces OA-induced steatosis in HepG2 cells by reducing fatty acid uptake and transport via FABP1 downregulation.</p><h2>Other Information</h2><p dir="ltr">Published in: Scientific Reports<br>License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1038/s41598-022-06143-5" target="_blank">https://dx.doi.org/10.1038/s41598-022-06143-5</a></p>2022-02-09T03:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1038/s41598-022-06143-5https://figshare.com/articles/journal_contribution/Exendin-4_alleviates_steatosis_in_an_in_vitro_cell_model_by_lowering_FABP1_and_FOXA1_expression_via_the_Wnt_-catenin_signaling_pathway/25125068CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/251250682022-02-09T03:00:00Z
spellingShingle Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
Olfa Khalifa (10914452)
Biomedical and clinical sciences
Clinical sciences
Non-alcoholic fatty liver disease (NAFLD)
liver disease
diabetes
status_str publishedVersion
title Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
title_full Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
title_fullStr Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
title_full_unstemmed Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
title_short Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
title_sort Exendin-4 alleviates steatosis in an in vitro cell model by lowering FABP1 and FOXA1 expression via the Wnt/-catenin signaling pathway
topic Biomedical and clinical sciences
Clinical sciences
Non-alcoholic fatty liver disease (NAFLD)
liver disease
diabetes