Evidence map›Paper›PMID 21346097›Full record

ArticleThe Journal of nutrition2011

PPARalpha expression protects male mice from high fat-induced nonalcoholic fatty liver.

Mohamed A Abdelmegeed, Seong-Ho Yoo, Lauren E Henderson, Frank J Gonzalez, Kimberley J Woodcroft, Byoung-Joon Song

Abstract read
In one paragraph

Article in The Journal of nutrition, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
10.6field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 246 citations in OpenAlex.

  1. The Role of Cannabidiol in Liver Disease: A Systemic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Pooled it
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  6. Review
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  11. Ubiquitination and Metabolic Disease.Advances in experimental medicine and biology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Keratin 79 is a PPARA target that is highly expressed by liver damage.Biochemical and biophysical research communications · 2023
    Article
  18. Peptide Helix-YPPAR research · 2023
    Article
  19. Article
  20. Article

67 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Mohamed A AbdelmegeedLaboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA..
Seong-Ho Yoo
Lauren E Henderson
Frank J Gonzalez
Kimberley J Woodcroft
Byoung-Joon Song
National Institutes of Health · USHenry Ford Health System · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
Alcohol Metabolism, Functional Consequences, Apoptosis Signaling Pathways, and Organ DamageZIAAA000036 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI SONG, BYOUNG-JOON · 2009 to 2025
$14.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Emerging evidence suggests that the lack of PPARα enhances hepatic steatosis and inflammation in Ppara-null mice when fed a high-fat diet (HFD). Thus, the aim of this study was to determine whether Ppara-null mice are more susceptible to nonalcoholic steatohepatitis (NASH) than their wild-type (WT) counterparts following short-term feeding with a HFD. Age-matched male WT and Ppara-null mice were randomly assigned to consume ad libitum a standard Lieber-DeCarli liquid diet (STD) (35% energy from fat) or a HFD (71% energy from fat) for 3 wk. Liver histology, plasma transaminase levels, and indicators of oxidative/nitrosative stress and inflammatory cytokines were evaluated in all groups. Levels of lobular inflammation and the NASH activity score were greater in HFD-exposed Ppara-null mice than in the other 3 groups. Biochemical analysis revealed elevated levels of ethanol-inducible cytochrome P450 2E1 and TNFα accompanied by increased levels of malondialdehyde as well as oxidized and nitrated proteins in Ppara-null mice. Elevated oxidative stress and inflammation were associated with activation of c-Jun-N-terminal kinase and p38 kinase, resulting in increased hepatocyte apoptosis in Ppara-null mice fed a HFD. These results, with increased steatosis, oxidative stress, and inflammation observed in Ppara-null mice fed a HFD, demonstrate that inhibition of PPARα functions may increase susceptibility to high fat-induced NASH.

Indexed as

AnimalsApoptosisCytochrome P-450 CYP2E1Dietary FatsFatty LiverJNK Mitogen-Activated Protein KinasesLipid PeroxidationLiverMaleMiceNitric Oxide Synthase Type IINon-alcoholic Fatty Liver DiseaseOrgan Sizep38 Mitogen-Activated Protein KinasesPPAR alphaProteinsCytochrome P-450 CYP2E1Dietary FatsJNK Mitogen-Activated Protein KinasesNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesPPAR alphaProteinsTumor Necrosis Factor-alpha

Identifiers

PMID21346097
PMCPMC3056578
OpenAlexW2112317454

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.