Evidence map›Paper›PMID 30605883›Full record

ArticleRedox biology2019

Consumption of decaffeinated coffee protects against the development of early non-alcoholic steatohepatitis: Role of intestinal barrier function.

Annette Brandt, Anika Nier, Cheng Jun Jin, Anja Baumann, Finn Jung, Vicent Ribas, Carmen García-Ruiz, Jose C Fernández-Checa, Ina Bergheim

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Food science & nutrition · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Intestinal Barrier in Human Health and Disease.International journal of environmental research and public health · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. 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

9 authors at 4 institutions in 4 countries.

Annette BrandtDepartment of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.
Anika NierDepartment of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.
Cheng Jun JinInstitute of Nutrition, SD Model Systems of Molecular Nutrition, Friedrich-Schiller University Jena, Jena, Germany.
Anja BaumannDepartment of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.
Finn JungDepartment of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.
Vicent RibasCell Death and Proliferation, Institute of Biomedical Research of Barcelona, Spanish National Research Council, Barcelona, Spain; Liver Unit, Clinical and Provincial Hospital of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and CIBEREHD, Barcelona, Spain.
Carmen García-RuizCell Death and Proliferation, Institute of Biomedical Research of Barcelona, Spanish National Research Council, Barcelona, Spain; Liver Unit, Clinical and Provincial Hospital of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and CIBEREHD, Barcelona, Spain; Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Jose C Fernández-ChecaCell Death and Proliferation, Institute of Biomedical Research of Barcelona, Spanish National Research Council, Barcelona, Spain; Liver Unit, Clinical and Provincial Hospital of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and CIBEREHD, Barcelona, Spain; Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Ina BergheimDepartment of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria. Electronic address: ina.bergheim@univie.ac.at.
University of Vienna · ATUniversity of Southern California · USCentro de Investigación Biomédica en Red · ESFriedrich Schiller University Jena · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide lacking universally accepted therapies. Studies suggest that coffee consumption is associated with a reduced risk of NAFLD; however, molecular mechanisms and ingredients involved remain to be fully understood. Here, we determined the effects of regular intake of decaffeinated coffee on the development of NAFLD in mice, and molecular mechanisms involved.

methodsFemale C57BL/6J mice (n = 6-7/ group) were pair-fed either a liquid control diet (C) or fat-, fructose- and cholesterol-rich diet (FFC) +/- decaffeinated coffee (DeCaf, 6 g/kg BW) for 4 days or 6 weeks. Indices of liver damage, hepatic inflammation and parameters of insulin resistance and intestinal permeability as well as nitric oxide system were determined.

resultsEarly signs of insulin resistance and non-alcoholic steatohepatitis (NASH) found after 6 weeks of FFC feeding were significantly lower in FFC+DeCaf-fed mice when compared to FFC-fed animals. Moreover, elevation of portal endotoxin levels and loss of tight junction proteins in proximal small intestine found in FFC-fed mice were significantly attenuated in FFC+DeCaf-fed animals. These beneficial effects of DeCaf were associated with a protection against the significant induction of inducible NO-synthase protein levels and 3-nitrotyrosine protein adducts found in proximal small intestine of FFC-fed mice. Similar protective effects of DeCaf were also found in mice fed the FFC diet short-term.

conclusionOur results suggest that protective effects of DeCaf on the development of NAFLD are at least in part related to maintaining intestinal barrier function.

Indexed as

CoffeeFeeding BehaviorAnimalsBiomarkersEndoplasmic Reticulum StressFemaleGlucoseImmunohistochemistryIntestinal MucosaLipid PeroxidationLiverMiceNitric OxideNon-alcoholic Fatty Liver DiseasePermeabilityToll-Like Receptor 4BiomarkersCoffeeGlucoseNitric OxideToll-Like Receptor 4CoffeeFatty liverInflammationiNOSIntestinal permeability

Identifiers

PMID30605883
PMCPMC6313826
OpenAlexW2906612208

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.