Evidence map›Paper›PMID 31767938›Full record

ArticleScientific reports2019

Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease.

Muhammad Ashfaq-Khan, Misbah Aslam, Muhammad Asif Qureshi, Marcel Sascha Senkowski, Shih Yen-Weng, Susanne Strand, Yong Ook Kim, Geethanjali Pickert, Jörn M Schattenberg, Detlef Schuppan

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
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  8. Genetic architecture underlying the expression of eight α-amylase trypsin inhibitors.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2021
    Article
  9. Immunonutritional Protease Inhibitors fromInternational journal of molecular sciences · 2021
    Article
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  11. Review
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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

10 authors at 3 institutions in 2 countries.

Muhammad Ashfaq-KhanInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Misbah AslamInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Muhammad Asif QureshiInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Marcel Sascha SenkowskiInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Shih Yen-WengInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Susanne StrandDepartment of Medicine I, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Yong Ook KimInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Geethanjali PickertInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Jörn M SchattenbergDepartment of Medicine I, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Detlef SchuppanInstitute of Translational Immunology and Research Center for Immune Therapy, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany. detlef.schuppan@unimedizin-mainz.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DEBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated that a common dietary protein component, wheat amylase trypsin inhibitors (ATI), stimulate intestinal macrophages and dendritic cells via toll like receptor 4. Activation of these intestinal myeloid cells elicits an inflammatory signal that is propagated to mesenteric lymph nodes, and that can facilitate extraintestinal inflammation. Mice were fed a well-defined high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amounts of ATI. Mice on HFD/ATI developed only mild signs of intestinal inflammation and myeloid cell activation but displayed significantly higher serum triglycerides and transaminases compared to mice on HFD alone. Moreover, they showed increased visceral and liver fat, and a higher insulin resistance. ATI feeding promoted liver and adipose tissue inflammation, with M1-type macrophage polarization and infiltration, and enhanced liver fibrogenesis. Gluten, the major protein component of wheat, did not induce these pathologies. Therefore, wheat ATI ingestion in minute quantities comparable to human daily wheat consumption exacerbated features of the metabolic syndrome and non-alcoholic steatohepatitis, despite its irrelevant caloric value.

Indexed as

Alanine TransaminaseAnimal FeedAnimalsCollagenDiet, Fat-RestrictedDiet, High-FatGene Expression ProfilingGlucose Tolerance TestGlutensHypertriglyceridemiaInflammationInsulinInsulin ResistanceIntra-Abdominal FatLiver CirrhosisMaleAlanine TransaminaseCollagenGlutensInsulinTrypsin InhibitorsZein

Identifiers

PMID31767938
PMCPMC6877510
OpenAlexW2989710419

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.