Genes, Vol. 12, Pages 1439: The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease

Genes, Vol. 12, Pages 1439: The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease Genes doi: 10.3390/genes12091439 Authors: Guglielmina Chimienti Antonella Orlando Francesco Russo Benedetta D’Attoma Manuela Aragno Eleonora Aimaretti Angela Maria Serena Lezza Vito Pesce 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 p...
Source: Genes - Category: Genetics & Stem Cells Authors: Tags: Article Source Type: research