Evidence map›Paper›PMID 25447846›Full record

ArticleGastroenterology2015

Alcohol disrupts levels and function of the cystic fibrosis transmembrane conductance regulator to promote development of pancreatitis.

József Maléth, Anita Balázs, Petra Pallagi, Zsolt Balla, Balázs Kui, Máté Katona, Linda Judák, István Németh, Lajos V Kemény, Zoltán Rakonczay and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 4 pooled it
16.4field-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

87 citing papers in PubMed, 4 syntheses or guidelines pooled it, 196 citations in OpenAlex.

  1. Pooled it
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  12. Article
  13. Treatment Strategies for Chronic Pancreatitis (CP).Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  14. Review
  15. Diagnosis and Management of Acute Pancreatitis.Diagnostics (Basel, Switzerland) · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 9 institutions in 5 countries.

József MaléthFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Anita BalázsFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Petra PallagiFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Zsolt BallaFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Balázs KuiFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Máté KatonaFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Linda JudákFirst Department of Medicine, University of Szeged, Szeged, Hungary; Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary.
István NémethDepartment of Dermatology and Allergology, University of Szeged, Szeged, Hungary.
Lajos V KeményFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Zoltán RakonczayFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Viktória VengloveczDepartment of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary.
Imre FöldesiDepartment of Laboratory Medicine, University of Szeged, Szeged, Hungary.
Zoltán PetőDepartment of Emergency Medicine, University of Szeged, Szeged, Hungary.
Áron SomoráczSecond Department of Pathology, Semmelweis University, Budapest, Hungary.
Katalin BorkaSecond Department of Pathology, Semmelweis University, Budapest, Hungary.
Doranda PerdomoDepartment of Physiology, McGill University, Montreal, Quebec, Canada.
Gergely L LukacsDepartment of Physiology, McGill University, Montreal, Quebec, Canada.
Mike A GrayInstitute for Cell & Molecular Biosciences, Newcastle University, Newcastle upon Tyne, England.
Stefania MonterisiDepartment of Physiology, Anatomy and Genetics, Oxford University, Oxford, England.
Manuela ZaccoloDepartment of Physiology, Anatomy and Genetics, Oxford University, Oxford, England.
Matthias SendlerDepartment of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Julia MayerleDepartment of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Jens-Peter KühnInstitute of Radiology, University Medicine, Ernst Moritz University, Greifswald, Germany.
Markus M LerchDepartment of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Miklós Sahin-TóthDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, Massachusetts.
Péter HegyiFirst Department of Medicine, University of Szeged, Szeged, Hungary; MTA-SZTE Lendület Translational Gastroenterology Research Group, Szeged, Hungary. Electronic address: hegyi.peter@med.u-szeged.hu.
University of Szeged · HUUniversitätsmedizin Greifswald · DEMcGill University · CASemmelweis University · HUUniversity of Oxford · GBBoston University · USMTA-SZTE Research Group on Artificial Intelligence · HUNewcastle University · GBUniversität Greifswald · DE

Funding

Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
British Heart Foundation RG/12/3/29423NIDDK NIH HHS R01 DK058088
6 · The paper itself

Abstract

BACKGROUND &

aimsExcessive consumption of ethanol is one of the most common causes of acute and chronic pancreatitis. Alterations to the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) also cause pancreatitis. However, little is known about the role of CFTR in the pathogenesis of alcohol-induced pancreatitis.

methodsWe measured CFTR activity based on chloride concentrations in sweat from patients with cystic fibrosis, patients admitted to the emergency department because of excessive alcohol consumption, and healthy volunteers. We measured CFTR levels and localization in pancreatic tissues and in patients with acute or chronic pancreatitis induced by alcohol. We studied the effects of ethanol, fatty acids, and fatty acid ethyl esters on secretion of pancreatic fluid and HCO3(-), levels and function of CFTR, and exchange of Cl(-) for HCO3(-) in pancreatic cell lines as well as in tissues from guinea pigs and CFTR knockout mice after administration of alcohol.

resultsChloride concentrations increased in sweat samples from patients who acutely abused alcohol but not in samples from healthy volunteers, indicating that alcohol affects CFTR function. Pancreatic tissues from patients with acute or chronic pancreatitis had lower levels of CFTR than tissues from healthy volunteers. Alcohol and fatty acids inhibited secretion of fluid and HCO3(-), as well as CFTR activity, in pancreatic ductal epithelial cells. These effects were mediated by sustained increases in concentrations of intracellular calcium and adenosine 3',5'-cyclic monophosphate, depletion of adenosine triphosphate, and depolarization of mitochondrial membranes. In pancreatic cell lines and pancreatic tissues of mice and guinea pigs, administration of ethanol reduced expression of CFTR messenger RNA, reduced the stability of CFTR at the cell surface, and disrupted folding of CFTR at the endoplasmic reticulum. CFTR knockout mice given ethanol or fatty acids developed more severe pancreatitis than mice not given ethanol or fatty acids.

conclusionsBased on studies of human, mouse, and guinea pig pancreata, alcohol disrupts expression and localization of the CFTR. This appears to contribute to development of pancreatitis. Strategies to increase CFTR levels or function might be used to treat alcohol-associated pancreatitis.

Indexed as

Adenosine TriphosphateAnimalsBicarbonatesCalciumChloride ChannelsCystic Fibrosis Transmembrane Conductance RegulatorEthanolGuinea PigsHumansMiceMutationPancreatitisProtein FoldingAdenosine TriphosphateBicarbonatesCalciumChloride ChannelsCystic Fibrosis Transmembrane Conductance RegulatorEthanolAlcoholismCl(−) ChannelDuctExocrine Pancreas

Identifiers

PMID25447846
PMCPMC4353632
OpenAlexW2004536546

What OpenQuestion holds

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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.