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The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the...

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Autores principales: Chimienti, Guglielmina, Orlando, Antonella, Russo, Francesco, D’Attoma, Benedetta, Aragno, Manuela, Aimaretti, Eleonora, Lezza, Angela Maria Serena, Pesce, Vito
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471525/
https://www.ncbi.nlm.nih.gov/pubmed/34573421
http://dx.doi.org/10.3390/genes12091439
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author Chimienti, Guglielmina
Orlando, Antonella
Russo, Francesco
D’Attoma, Benedetta
Aragno, Manuela
Aimaretti, Eleonora
Lezza, Angela Maria Serena
Pesce, Vito
author_facet Chimienti, Guglielmina
Orlando, Antonella
Russo, Francesco
D’Attoma, Benedetta
Aragno, Manuela
Aimaretti, Eleonora
Lezza, Angela Maria Serena
Pesce, Vito
author_sort Chimienti, Guglielmina
collection PubMed
description Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence and effects of mitochondrial oxidative stress in the liver from rats fed a high-fat plus fructose (HF-F) diet inducing NAFLD. Supplementation with dehydroepiandrosterone (DHEA), a multitarget antioxidant, was tested for efficacy in delaying NAFLD. A marked mitochondrial oxidative stress was originated by all diets, as demonstrated by the decrease in Superoxide Dismutase 2 (SOD2) and Peroxiredoxin III (PrxIII) amounts. All diets induced a decrease in mitochondrial DNA content and an increase in its oxidative damage. The diets negatively affected mitochondrial biogenesis as shown by decreased peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), mitochondrial transcription factor A (TFAM), and the COX-IV subunit from the cytochrome c oxidase complex. The reduced amounts of Beclin-1 and lipidated LC3 II form of the microtubule-associated protein 1 light chain 3 (LC3) unveiled the diet-related autophagy’s decrease. The DHEA supplementation did not prevent the diet-induced changes. These results demonstrate the relevance of mitochondrial oxidative stress and the sequential dysfunction of the organelles in an obesogenic diet animal model of NAFLD.
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spelling pubmed-84715252021-09-28 The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease Chimienti, Guglielmina Orlando, Antonella Russo, Francesco D’Attoma, Benedetta Aragno, Manuela Aimaretti, Eleonora Lezza, Angela Maria Serena Pesce, Vito Genes (Basel) Article Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence and effects of mitochondrial oxidative stress in the liver from rats fed a high-fat plus fructose (HF-F) diet inducing NAFLD. Supplementation with dehydroepiandrosterone (DHEA), a multitarget antioxidant, was tested for efficacy in delaying NAFLD. A marked mitochondrial oxidative stress was originated by all diets, as demonstrated by the decrease in Superoxide Dismutase 2 (SOD2) and Peroxiredoxin III (PrxIII) amounts. All diets induced a decrease in mitochondrial DNA content and an increase in its oxidative damage. The diets negatively affected mitochondrial biogenesis as shown by decreased peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), mitochondrial transcription factor A (TFAM), and the COX-IV subunit from the cytochrome c oxidase complex. The reduced amounts of Beclin-1 and lipidated LC3 II form of the microtubule-associated protein 1 light chain 3 (LC3) unveiled the diet-related autophagy’s decrease. The DHEA supplementation did not prevent the diet-induced changes. These results demonstrate the relevance of mitochondrial oxidative stress and the sequential dysfunction of the organelles in an obesogenic diet animal model of NAFLD. MDPI 2021-09-18 /pmc/articles/PMC8471525/ /pubmed/34573421 http://dx.doi.org/10.3390/genes12091439 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Chimienti, Guglielmina
Orlando, Antonella
Russo, Francesco
D’Attoma, Benedetta
Aragno, Manuela
Aimaretti, Eleonora
Lezza, Angela Maria Serena
Pesce, Vito
The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title_full The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title_fullStr The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title_full_unstemmed The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title_short The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
title_sort mitochondrial trigger in an animal model of nonalcoholic fatty liver disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471525/
https://www.ncbi.nlm.nih.gov/pubmed/34573421
http://dx.doi.org/10.3390/genes12091439
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