Evidence map›Paper›PMID 23948742›Full record

ArticlePflugers Archiv : European journal of physiology2014

Ethanol and its non-oxidative metabolites profoundly inhibit CFTR function in pancreatic epithelial cells which is prevented by ATP supplementation.

L Judák, P Hegyi, Z Rakonczay, J Maléth, M A Gray, V Venglovecz

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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Review
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  9. Review
  10. Intracellular CaInternational journal of molecular sciences · 2020
    Review
  11. Review
  12. A NovelFrontiers in physiology · 2019
    Article
  13. Article
  14. Article
  15. Review
  16. Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017
    Review
  17. Ca2+ toxicity and mitochondrial damage in acute pancreatitis: translational overview.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  18. Article
  19. Review
  20. CFTR: A New Horizon in the Pathomechanism and Treatment of Pancreatitis.Reviews of physiology, biochemistry and pharmacology · 2016
    Review
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 2 countries.

L JudákDepartment of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary.
P Hegyi
Z Rakonczay
J Maléth
M A Gray
V Venglovecz
University of Szeged · HUNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive alcohol consumption is a major cause of acute pancreatitis, but the mechanism involved is not well understood. Recent investigations suggest that pancreatic ductal epithelial cells (PDECs) help defend the pancreas from noxious agents such as alcohol. Because the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel plays a major role in PDEC physiology and mutated CFTR is often associated with pancreatitis, we tested the hypothesis that ethanol affects CFTR to impair ductal function. Electrophysiological studies on native PDECs showed that ethanol (10 and 100 mM) increased basal, but reversibly blocked, forskolin-stimulated CFTR currents. The inhibitory effect of ethanol was mimicked by its non-oxidative metabolites, palmitoleic acid ethyl ester (POAEE) and palmitoleic acid (POA), but not by the oxidative metabolite, acetaldehyde. Ethanol, POAEE and POA markedly reduced intracellular ATP (ATPi) which was linked to CFTR inhibition since the inhibitory effects were almost completely abolished if ATPi depletion was prevented. We propose that ethanol causes functional damage of CFTR through an ATPi-dependent mechanism, which compromises ductal fluid secretion and likely contributes to the pathogenesis of acute pancreatitis. We suggest that the maintenance of ATPi may represent a therapeutic option in the treatment of the disease.

Indexed as

AcetaldehydeAction PotentialsAdenosine TriphosphateAnimalsCell Line, TumorCells, CulturedCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsEthanolFatty Acids, MonounsaturatedGuinea PigsHumansPancreatic DuctsAcetaldehydeAdenosine TriphosphateCystic Fibrosis Transmembrane Conductance RegulatorEthanolFatty Acids, Monounsaturatedpalmitoleic acid

Identifiers

PMID23948742
OpenAlexW2063812527

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.