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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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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. |
format | Online Article Text |
id | pubmed-8471525 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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