Evidence map›Paper›PMID 34869528›Full record

ArticleFrontiers in nutrition2021

Long-Term Overconsumption of Fat and Sugar Causes a Partially Reversible Pre-inflammatory Bowel Disease State.

Djésia Arnone, Marie Vallier, Sébastien Hergalant, Caroline Chabot, Ndeye Coumba Ndiaye, David Moulin, Anda-Maria Aignatoaei, Jean-Marc Alberto, Huguette Louis, Olivier Boulard and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in nutrition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  6. Effects and mechanism ofWorld journal of gastroenterology · 2026
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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

19 authors at 5 institutions in 2 countries.

Djésia ArnoneInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Marie VallierSection of Evolutionary Medicine, Institute for Experimental Medicine, Kiel University and Max Planck Institute for Evolutionary Biology, Plön, Germany.
Sébastien HergalantInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Caroline ChabotCHRU-Nancy, Pediatric Hepato-Gastroenterology and Nutrition Unit, Department of Child Medicine and Clinical Genetics, Inserm U1256, Université de Lorraine, Nancy, France.
Ndeye Coumba NdiayeInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
David MoulinIMoPA, UMR7365 CNRS-Université de Lorraine, CHRU de Nancy, Contrat d'interface, Nancy, France.
Anda-Maria AignatoaeiDepartment of Anatomopathology, CHRU de Nancy, Nancy, France.
Jean-Marc AlbertoInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Huguette LouisDepartment Inserm UMRS_1116 DCAC, Université de Lorraine, Nancy, France.
Olivier BoulardLaboratory of Cell Physiology, INSERM U1003, University of Lille, Lille, France.
Camille MayeurMicalis Institute, INRAE, AgroParisTech, Université Paris-Saclay, Jouy-en-Josas, France.
Natacha DreumontInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Kenneth PeukerCenter for Regenerative Therapies, Technische Universität (TU) Dresden, Dresden, Germany.
Anne StrigliCenter for Regenerative Therapies, Technische Universität (TU) Dresden, Dresden, Germany.
Sebastian ZeissigCenter for Regenerative Therapies, Technische Universität (TU) Dresden, Dresden, Germany.
Franck HansmannelInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Matthias ChamaillardLaboratory of Cell Physiology, INSERM U1003, University of Lille, Lille, France.
Tunay KöktenInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Laurent Peyrin-BirouletInserm U1256, Nutrition Genetics and Exposition NGERE, Université de Lorraine, Nancy, France.
Inserm · FRTechnische Universität Dresden · DECentre National de la Recherche Scientifique · FRAgroParisTech · FRMax Planck Institute for Evolutionary Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nutrition appears to be an important environmental factor involved in the onset of inflammatory bowel diseases (IBD) through yet poorly understood biological mechanisms. Most studies focused on fat content in high caloric diets, while refined sugars represent up to 40% of caloric intake within industrialized countries and contribute to the growing epidemics of inflammatory diseases. Herein we aim to better understand the impact of a high-fat-high-sucrose diet on intestinal homeostasis in healthy conditions and the subsequent colitis risk. We investigated the early events and the potential reversibility of high caloric diet-induced damage in mice before experimental colitis. C57BL/6 mice were fed with a high-fat or high-fat high-sucrose or control diet before experimental colitis. In healthy mice, a high-fat high-sucrose diet induces a pre-IBD state characterized by gut microbiota dysbiosis with a total depletion of bacteria belonging to Barnesiella that is associated with subclinical endoscopic lesions. An overall down-regulation of the colonic transcriptome converged with broadly decreased immune cell populations in the mesenteric lymph nodes leading to the inability to respond to tissue injury. Such

Indexed as

colitisdiet-inducedgut homeostasishigh-fat high-sucrose dietIBD-inflammatory bowel diseases

Identifiers

PMID34869528
PMCPMC8637418
OpenAlexW3212280067

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.