Evidence map›Paper›PMID 35906289›Full record

ReviewNature reviews. Gastroenterology & hepatology2022

The metabolic nature of inflammatory bowel diseases.

Timon E Adolph, Moritz Meyer, Julian Schwärzler, Lisa Mayr, Felix Grabherr, Herbert Tilg

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06352515 (Peripheral Blood T Lymphocyte Subsets in Ulcerative Colitis), which is not on this map. Cited by 148 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 4 pooled it
21.3field-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.

NCT06352515 not yet recruitingnot on this mapstarted 2024, after this paper: background citation

Peripheral Blood T Lymphocyte Subsets in Ulcerative Colitis

TypeobservationalSponsorAssiut UniversityRan2024 to 2027Enrolled80ConditionsUlcerative ColitisArmsFlow cytometry
3 · Its place in the literature

Who cites it

148 citing papers in PubMed, 4 syntheses or guidelines pooled it, 267 citations in OpenAlex.

  1. Pooled it
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  4. Debate on the relationship betweenFrontiers in microbiology · 2024
    Pooled it
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88 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

6 authors at 1 institution in 1 country.

Timon E AdolphDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria. timon-erik.adolph@i-med.ac.at.ORCID 0000-0002-4736-830X
Moritz MeyerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Julian SchwärzlerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Lisa MayrDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Felix GrabherrDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.ORCID 0000-0001-5731-8253
Herbert TilgDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria. herbert.tilg@i-med.ac.at.ORCID 0000-0002-4235-2579
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF P 29379Austrian Science Fund FWF P 33070
6 · The paper itself

Abstract

Crohn's disease and ulcerative colitis, phenotypically comprising a spectrum of inflammatory bowel diseases (IBDs), spread globally during the westernization of lifestyle and dietary habits over the past few decades. Here, we review experimental and clinical evidence for the metabolic nature of gut inflammation in IBD and delineate distinct parallels to the inflammatory state in metabolic diseases. Experimental evidence indicates that excessive intake of specific macronutrients in a Western diet fuels an inflammatory response in the gut by exploiting sensors of innate immunity and perturbation of gut microbial metabolism. Genetic IBD risk partly affects metabolism and stress signalling of innate immunity, and immunometabolism controls susceptibility to gut inflammation. Epidemiological and clinical studies indicate that specific nutrients in the Western diet pose a risk for the development of IBD and a poor disease course. Translational studies in IBD indicate perturbation of energy metabolism in immune cells and perturbation of gut microbial metabolism, which can be shaped by diet. In turn, dietary restriction by exclusive enteral nutrition induces remission in patients with IBD. Collectively, these studies support a metabolic underpinning of gut inflammation in IBD as described for metabolic inflammation in obesity and related disorders.

Indexed as

Colitis, UlcerativeCrohn DiseaseInflammatory Bowel DiseasesDietHumansInflammation

Identifiers

PMID35906289
OpenAlexW4288689706

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.