Evidence map›Paper›PMID 34573421›Full record

ArticleGenes2021

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

Guglielmina Chimienti, Antonella Orlando, Francesco Russo, Benedetta D'Attoma, Manuela Aragno, Eleonora Aimaretti, Angela Maria Serena Lezza, Vito Pesce

Open access · goldAbstract read
In one paragraph

Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Guglielmina ChimientiDepartment of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari Aldo Moro, Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-4403-2317
Antonella OrlandoLaboratory of Nutritional Pathophysiology, National Institute of Gastroenterology "S. de Bellis" Research Hospital, Castellana Grotte, 70013 Bari, Italy.ORCID 0000-0001-8255-4776
Francesco RussoLaboratory of Nutritional Pathophysiology, National Institute of Gastroenterology "S. de Bellis" Research Hospital, Castellana Grotte, 70013 Bari, Italy.ORCID 0000-0003-0538-6072
Benedetta D'AttomaLaboratory of Nutritional Pathophysiology, National Institute of Gastroenterology "S. de Bellis" Research Hospital, Castellana Grotte, 70013 Bari, Italy.
Manuela AragnoDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125 Torino, Italy.ORCID 0000-0002-0453-5235
Eleonora AimarettiDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125 Torino, Italy.ORCID 0000-0001-6336-1442
Angela Maria Serena LezzaDepartment of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari Aldo Moro, Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-2006-1076
Vito PesceDepartment of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari Aldo Moro, Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-9148-3129
Gastroenterology Hospital "Saverio de Bellis" · ITUniversity of Bari Aldo Moro · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAntioxidantsAutophagyDehydroepiandrosteroneDiet, High-FatDisease Models, AnimalDNA, MitochondrialMaleMitochondria, LiverNon-alcoholic Fatty Liver DiseaseOxidative StressPeroxiredoxin IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, WistarSuperoxide DismutaseAntioxidantsDehydroepiandrosteroneDNA, MitochondrialPeroxiredoxin IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratSuperoxide DismutaseSuperoxide Dismutase 2Tfam protein, ratTranscription FactorsDHEAhigh fat-fructose dietmitochondrial biogenesismtDNA damageNAFLD

Identifiers

PMID34573421
PMCPMC8471525
OpenAlexW3201186891

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.