Evidence map›Paper›PMID 31211831›Full record

ArticleInflammatory bowel diseases2020

Intestinal Inflammation Modulates the Epithelial Response to Butyrate in Patients With Inflammatory Bowel Disease.

Elena Ferrer-Picón, Isabella Dotti, Ana M Corraliza, Aida Mayorgas, Miriam Esteller, José Carlos Perales, Elena Ricart, Maria C Masamunt, Anna Carrasco, Eva Tristán and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 3 pooled it
12.5field-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

78 citing papers in PubMed, 3 syntheses or guidelines pooled it, 146 citations in OpenAlex.

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18 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

12 authors at 3 institutions in 1 country.

Elena Ferrer-PicónDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Isabella DottiDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Ana M CorralizaDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Aida MayorgasDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Miriam EstellerDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
José Carlos PeralesDepartment of Physiological Sciences, Faculty of Medicine, University of Barcelona, L'Hospitalet del Llobregat, Barcelona, Spain.
Elena RicartDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Maria C MasamuntDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Anna CarrascoDepartment of Gastroenterology, Hospital Universitari Mútua Terrassa, CIBERehd, Barcelona, Spain.
Eva TristánDepartment of Gastroenterology, Hospital Universitari Mútua Terrassa, CIBERehd, Barcelona, Spain.
Maria EsteveDepartment of Gastroenterology, Hospital Universitari Mútua Terrassa, CIBERehd, Barcelona, Spain.
Azucena SalasDepartment of Gastroenterology, IDIBAPS, Hospital Clínic, CIBERehd, Barcelona, Spain.
Hospital Clínic de Barcelona · ESMútua Terrassa · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundButyrate-producing gut bacteria are reduced in patients with active inflammatory bowel disease (IBD), supporting the hypothesis that butyrate supplementation may be beneficial in this setting. Nonetheless, earlier studies suggest that the oxidation of butyrate in IBD patients is altered. We propose that inflammation may decrease epithelial butyrate consumption.

methodsNon-IBD controls and IBD patients were recruited for the study. Stool samples were used for short-chain fatty acid and bacterial butyryl CoA:acetate CoA-transferase quantification. Colonic biopsies and ex vivo differentiated epithelial organoids (d-EpOCs) treated with butyrate and/or tumor necrosis factor alpha (TNFα) were used for analyzing the expression of transporters MCT1 and ABCG2, metabolic enzyme ACADS, and butyrate receptor GPR43, and for butyrate metabolism and consumption assays.

resultsWe observed that lower stool content of butyrate-producing bacteria in active IBD patients did not correlate with decreased butyrate concentrations. Indeed, the intestinal epithelial expression of MCT1, ABCG2, ACADS, and GPR43 was altered in active IBD patients. Nonetheless, d-EpOCs derived from IBD patients showed SLC16A1 (gene encoding for MCT1 protein), ABCG2, ACADS, and GPR43 expression levels comparable to controls. Moreover, IBD- and non-IBD-derived d-EpOCs responded similarly to butyrate, as assessed by transcriptional regulation. TNFα significantly altered SLC16A1, ABCG2, and GPR43 transcription in d-EpOCs, mimicking the expression profile observed in biopsies from active IBD patients and resulting in reduced butyrate consumption.

conclusionsWe provide evidence that the response to butyrate is not intrinsically altered in IBD patients. However, TNFα renders the epithelium less responsive to this metabolite, defeating the purpose of butyrate supplementation during active inflammation.

Indexed as

AdultAgedAged, 80 and overBiopsyButyratesCase-Control StudiesCell Culture TechniquesColitis, UlcerativeCrohn DiseaseFecesFemaleHumansInflammationInflammatory Bowel DiseasesIntestinal MucosaIntestinesButyratesTumor Necrosis Factor-alphabacterial metabolitesCrohn’s diseasehuman organoidsTNFαulcerative colitis

Identifiers

PMID31211831
PMCPMC6905302
OpenAlexW2951095666

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.