Evidence map›Paper›PMID 33505147›Full record

ReviewWorld journal of gastroenterology2021

Experimental models of metabolic and alcoholic fatty liver disease.

Delfin Gerard Buyco, Jasmin Martin, Sookyoung Jeon, Royce Hooks, Chelsea Lin, Rotonya Carr

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Gene-based therapies for steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  11. Article
  12. Article
  13. Effect ofWorld journal of gastroenterology · 2024
    Article
  14. Article
  15. Efficacy ofHeliyon · 2024
    Article
  16. Review
  17. Inhibitory Effects ofFoods (Basel, Switzerland) · 2024
    Article
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Delfin Gerard BuycoDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States.
Jasmin MartinDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States.
Sookyoung JeonDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States.
Royce HooksDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States.
Chelsea LinDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States.
Rotonya CarrDivision of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States. rotonya.carr@pennmedicine.upenn.edu.
University of Pennsylvania · US

Funding

Molecular Mechanisms Of Post-Transplant Recurrent Alcoholic Liver DiseaseR01AA026302 · NIAAA · UNIVERSITY OF WASHINGTON · PI ROTONYA M CARR · 2017 to 2026
$3.2M
NIAAA NIH HHS R01 AA026302
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a multi-systemic disease that is considered the hepatic manifestation of metabolic syndrome (MetS). Because alcohol consumption in NAFLD patients is common, there is a significant overlap in the pathogenesis of NAFLD and alcoholic liver disease (ALD). Indeed, MetS also significantly contributes to liver injury in ALD patients. This "syndrome of metabolic and alcoholic steatohepatitis" (SMASH) is thus expected to be a more prevalent presentation in liver patients, as the obesity epidemic continues. Several pre-clinical experimental models that couple alcohol consumption with NAFLD-inducing diet or genetic obesity have been developed to better understand the pathogenic mechanisms of SMASH. These models indicate that concomitant MetS and alcohol contribute to lipid dysregulation, oxidative stress, and the induction of innate immune response. There are significant limitations in the applicability of these models to human disease, such as the ability to induce advanced liver injury or replicate patterns in human food/alcohol consumption. Thus, there remains a need to develop models that accurately replicate patterns of obesogenic diet and alcohol consumption in SMASH patients.

Indexed as

Fatty Liver, AlcoholicLiver Diseases, AlcoholicMetabolic SyndromeNon-alcoholic Fatty Liver DiseaseHumansLiverModels, TheoreticalAlcoholic liver diseaseAnimal modelsInsulin resistanceNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisOxidative stress

Identifiers

PMID33505147
PMCPMC7789066
OpenAlexW3113451196

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.