Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/105529
DC Field | Value | Language |
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dc.contributor.author | Simoes, Ines C M | - |
dc.contributor.author | Karkucinska-Wieckowska, Agnieszka | - |
dc.contributor.author | Janikiewicz, Justyna | - |
dc.contributor.author | Szymanska, Sylwia | - |
dc.contributor.author | Pronicki, Maciej | - |
dc.contributor.author | Dobrzyn, Pawel | - |
dc.contributor.author | Dabrowski, Michal | - |
dc.contributor.author | Dobrzyn, Agnieszka | - |
dc.contributor.author | Oliveira, Paulo J. | - |
dc.contributor.author | Zischka, Hans | - |
dc.contributor.author | Potes, Yaiza | - |
dc.contributor.author | Wieckowski, Mariusz R. | - |
dc.date.accessioned | 2023-03-06T10:40:00Z | - |
dc.date.available | 2023-03-06T10:40:00Z | - |
dc.date.issued | 2020-10-15 | - |
dc.identifier.issn | 2076-3921 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/105529 | - |
dc.description.abstract | Nonalcoholic fatty liver disease (NAFLD) is characterized by the development of steatosis, which can ultimately compromise liver function. Mitochondria are key players in obesity-induced metabolic disorders; however, the distinct role of hypercaloric diet constituents in hepatic cellular oxidative stress and metabolism is unknown. Male mice were fed either a high-fat (HF) diet, a high-sucrose (HS) diet or a combined HF plus HS (HFHS) diet for 16 weeks. This study shows that hypercaloric diets caused steatosis; however, the HFHS diet induced severe fibrotic phenotype. At the mitochondrial level, lipidomic analysis showed an increased cardiolipin content for all tested diets. Despite this, no alterations were found in the coupling efficiency of oxidative phosphorylation and neither in mitochondrial fatty acid oxidation (FAO). Consistent with unchanged mitochondrial function, no alterations in mitochondrial-induced reactive oxygen species (ROS) and antioxidant capacity were found. In contrast, the HF and HS diets caused lipid peroxidation and provoked altered antioxidant enzyme levels/activities in liver tissue. Our work provides evidence that hepatic oxidative damage may be caused by augmented levels of peroxisomes and consequently higher peroxisomal FAO-induced ROS in the early NAFLD stage. Hepatic damage is also associated with autophagic flux impairment, which was demonstrated to be diet-type dependent. The HS diet induced a reduction in autophagosomal formation, while the HF diet reduced levels of cathepsins. The accumulation of damaged organelles could instigate hepatocyte injuries and NAFLD progression. | pt |
dc.description.sponsorship | M.R.W., I.C.M.S. and Y.P. were supported by the National Science Centre, Poland (UMO-2018/29/B/NZ1/00589). H.Z. was supported by the Deutsche Forschungsgemeinschaft (DFG) (Grant ZI1386/2-1). P.J.O. is supported by FEDER funds through the Operational Program Competitiveness Factors COMPETE and national funds by the Foundation for Science and Technology (FCT) (Grants PTDC/ASP-HOR/29152/2017, POCI-01-0145-FEDER-029152 and UIDB/04539/2020). I.C.M.S., P.J.O., H.Z. and M.R.W. gratefully acknowledge the financial support for this research from the FOIE GRAS and mtFOIE GRAS projects. These projects received funding from the European Union’s Horizon 2020 Research and Innovation program under the Marie Skłodowska-Curie Grant Agreement No. 722619 (FOIE GRAS) and Grant Agreement No. 734719 (mtFOIE GRAS). | pt |
dc.language.iso | eng | pt |
dc.publisher | MDPI | pt |
dc.relation | PTDC/ASP-HOR/29152/2017 | pt |
dc.relation | UIDB/04539/2020 | pt |
dc.relation | info:eu-repo/grantAgreement/H2020/722619/EU/MarieSkłodowska-Curie/FOIEGRAS | pt |
dc.relation | Deutsche Forschungsgemeinschaft (DFG) | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject | mitochondria | pt |
dc.subject | oxidative stress | pt |
dc.subject | peroxisomes | pt |
dc.subject | autophagy | pt |
dc.subject | steatosis | pt |
dc.title | Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response | pt |
dc.type | article | - |
degois.publication.firstPage | 995 | pt |
degois.publication.issue | 10 | pt |
degois.publication.title | Antioxidants | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.3390/antiox9100995 | pt |
degois.publication.volume | 9 | pt |
dc.date.embargo | 2020-10-15 | * |
uc.date.periodoEmbargo | 0 | pt |
item.fulltext | Com Texto completo | - |
item.grantfulltext | open | - |
item.languageiso639-1 | en | - |
item.cerifentitytype | Publications | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
crisitem.project.grantno | VALORIZEBYPRODU Preclinical efficacy of sulforaphane or Brassica whole extract: a strategy to fight obesity and valorize Brassica byproducts | - |
crisitem.project.grantno | Center for Innovative Biomedicine and Biotechnology - CIBB | - |
crisitem.project.grantno | FOIE GRAS -Bioenergetic Remodeling in the Pathophysiology and Treatment of Non-Alcoholic Fatty Liver Disease | - |
crisitem.project.grantno | (DFG) | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0002-5201-9948 | - |
Appears in Collections: | I&D CNC - Artigos em Revistas Internacionais |
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Western-diet-causes-obesityinduced-nonalcoholic-fatty-liver-disease-development-by-differentially-compromising-the-autophagic-responseAntioxidants.pdf | 3.72 MB | Adobe PDF | View/Open |
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