The mitochondrial trigger in an animal model of nonalcoholic fatty liver disease
| Autor: | Vito Pesce, Francesco Russo, Eleonora Aimaretti, Angela Maria Serena Lezza, Antonella Orlando, Guglielmina Chimienti, Manuela Aragno, Benedetta D'Attoma |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_specialty Peroxiredoxin III mitochondrial biogenesis SOD2 Mitochondria Liver high fat-fructose diet QH426-470 medicine.disease_cause Diet High-Fat DNA Mitochondrial Antioxidants Article Superoxide dismutase Non-alcoholic Fatty Liver Disease Internal medicine NAFLD Nonalcoholic fatty liver disease Genetics medicine Autophagy Animals Rats Wistar DHEA Genetics (clinical) biology Chemistry Superoxide Dismutase Dehydroepiandrosterone TFAM medicine.disease High fructose diet Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Disease Models Animal Oxidative Stress Endocrinology Mitochondrial biogenesis biology.protein Steatosis mtDNA damage Oxidative stress Transcription Factors |
| Zdroj: | Genes Genes, Vol 12, Iss 1439, p 1439 (2021) Volume 12 Issue 9 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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