Evidence map›Paper›PMID 24162590›Full record

ArticleGut2014

Fatty acid ethyl ester synthase inhibition ameliorates ethanol-induced Ca2+-dependent mitochondrial dysfunction and acute pancreatitis.

Wei Huang, David M Booth, Matthew C Cane, Michael Chvanov, Muhammad A Javed, Victoria L Elliott, Jane A Armstrong, Hayley Dingsdale, Nicole Cash, Yan Li and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  5. Computed Tomography and Plasma Proteomics for Early Discrimination of Post-Pancreatitis Diabetes Mellitus.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. The Link between Alcohol Consumption and Kidney Injury.The American journal of pathology · 2026
    Review
  10. Article
  11. IL18 Works Like a Two-Side Coin in Acute Pancreatitis.International journal of general medicine · 2026
    Article
  12. Article
  13. Review
  14. Acute pancreatitis experimental models, advantages and disadvantages.Journal of physiology and biochemistry · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

44 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

18 authors at 4 institutions in 3 countries.

Wei HuangDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK NIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK Department of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Centre, West China Hospital, Sichuan University, China.
David M BoothDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Matthew C CaneDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Michael ChvanovDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK NIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Muhammad A JavedDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK NIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Victoria L ElliottNIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Jane A ArmstrongNIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Hayley DingsdaleDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Nicole CashDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Yan LiNIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
William GreenhalfNIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Rajarshi MukherjeeDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK NIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Bhupendra S KaphaliaDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Mohammed JaffarMorvus Technology Limited, Carmarthen, UK.
Ole H PetersenCardiff School of Biosciences, University of Cardiff, Cardiff, UK.
Alexei V TepikinDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
Robert SuttonNIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
David N CriddleDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK NIHR Liverpool Pancreas Biomedical Research Unit, RLBUHT, Institute of Translational Medicine, University of Liverpool, Liverpool, Merseyside, UK.
University of Liverpool · GBNIHR Liverpool Pancreatic Biomedical Research Unit · GBCardiff University · GBThe University of Texas Medical Branch at Galveston · US

Funding

Medical Research Council G0700167Medical Research Council G19/22Medical Research Council KO12967Medical Research Council MR/J002771/1Medical Research Council MR/K012967/1
6 · The paper itself

Abstract

objectiveNon-oxidative metabolism of ethanol (NOME) produces fatty acid ethyl esters (FAEEs) via carboxylester lipase (CEL) and other enzyme action implicated in mitochondrial injury and acute pancreatitis (AP). This study investigated the relative importance of oxidative and non-oxidative pathways in mitochondrial dysfunction, pancreatic damage and development of alcoholic AP, and whether deleterious effects of NOME are preventable.

designIntracellular calcium ([Ca(2+)](C)), NAD(P)H, mitochondrial membrane potential and activation of apoptotic and necrotic cell death pathways were examined in isolated pancreatic acinar cells in response to ethanol and/or palmitoleic acid (POA) in the presence or absence of 4-methylpyrazole (4-MP) to inhibit oxidative metabolism. A novel in vivo model of alcoholic AP induced by intraperitoneal administration of ethanol and POA was developed to assess the effects of manipulating alcohol metabolism.

resultsInhibition of OME with 4-MP converted predominantly transient [Ca(2+)](C) rises induced by low ethanol/POA combination to sustained elevations, with concurrent mitochondrial depolarisation, fall of NAD(P)H and cellular necrosis in vitro. All effects were prevented by 3-benzyl-6-chloro-2-pyrone (3-BCP), a CEL inhibitor. 3-BCP also significantly inhibited rises of pancreatic FAEE in vivo and ameliorated acute pancreatic damage and inflammation induced by administration of ethanol and POA to mice.

conclusionsA combination of low ethanol and fatty acid that did not exert deleterious effects per se became toxic when oxidative metabolism was inhibited. The in vitro and in vivo damage was markedly inhibited by blockade of CEL, indicating the potential for development of specific therapy for treatment of alcoholic AP via inhibition of FAEE generation.

Indexed as

Acinar CellsAcyltransferasesAnimalsApoptosisCalciumCalcium SignalingCarboxylesteraseCells, CulturedDisease Models, AnimalEthanolFatty AcidsFatty Acids, MonounsaturatedFomepizoleMembrane Potential, MitochondrialMiceMitochondria3-benzyl-6-chloro-2-pyroneAcyltransferasesCalciumCarboxylesteraseEthanolFatty AcidsFatty Acids, Monounsaturatedfatty acyl ethyl ester synthaseFomepizoleNADPpalmitoleic acidPyrazolesPyronesACUTE PancreatitisAlcohol-Induced InjuryCalciumEthanolPancreatic Damage

Identifiers

PMID24162590
PMCPMC4112447
OpenAlexW2122310415

What OpenQuestion 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 OpenQuestion graph.