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Open AccessArticle

Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response

1
Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland
2
Department of Pathology, The Children’s Memorial Health Institute, 04-730 Warsaw, Poland
3
CNC-Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, Biocant Park, 3060-197 Cantanhede, Portugal
4
Institute of Toxicology and Environmental Hygiene, School of Medicine, Technical University Munich, D-80802 Munich, Germany
5
Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, D-85764 Neuherberg, Germany
*
Authors to whom correspondence should be addressed.
These authors share senior authorship.
Antioxidants 2020, 9(10), 995; https://doi.org/10.3390/antiox9100995
Received: 28 September 2020 / Revised: 12 October 2020 / Accepted: 13 October 2020 / Published: 15 October 2020
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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. View Full-Text
Keywords: mitochondria; oxidative stress; peroxisomes; autophagy; steatosis mitochondria; oxidative stress; peroxisomes; autophagy; steatosis
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MDPI and ACS Style

Simoes, I.C.M.; Karkucinska-Wieckowska, A.; Janikiewicz, J.; Szymanska, S.; Pronicki, M.; Dobrzyn, P.; Dabrowski, M.; Dobrzyn, A.; Oliveira, P.J.; Zischka, H.; Potes, Y.; Wieckowski, M.R. Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response. Antioxidants 2020, 9, 995. https://doi.org/10.3390/antiox9100995

AMA Style

Simoes ICM, Karkucinska-Wieckowska A, Janikiewicz J, Szymanska S, Pronicki M, Dobrzyn P, Dabrowski M, Dobrzyn A, Oliveira PJ, Zischka H, Potes Y, Wieckowski MR. Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response. Antioxidants. 2020; 9(10):995. https://doi.org/10.3390/antiox9100995

Chicago/Turabian Style

Simoes, Ines C.M.; Karkucinska-Wieckowska, Agnieszka; Janikiewicz, Justyna; Szymanska, Sylwia; Pronicki, Maciej; Dobrzyn, Pawel; Dabrowski, Michal; Dobrzyn, Agnieszka; Oliveira, Paulo J.; Zischka, Hans; Potes, Yaiza; Wieckowski, Mariusz R. 2020. "Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response" Antioxidants 9, no. 10: 995. https://doi.org/10.3390/antiox9100995

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