Evidence map›Paper›PMID 41970986›Full record

ArticleFrontiers in endocrinology2026

Erika Kvalem Soto, Valeria Wagner, Julia Engl, Michael Mederer, Veronika Cibulkova, Johanna Piater, Benedikt Schäfer, Elena Dunzendorfer, Silvio Waschina, Susanne Kaser and 4 more

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

14 authors.

Erika Kvalem Soto *Biocenter, Institute of Bioinformatics, Medical University of Innsbruck, Innsbruck, Austria.
Valeria Wagner *Department of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Julia EnglDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Michael MedererDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Veronika CibulkovaDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Johanna PiaterDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Benedikt SchäferDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Elena DunzendorferDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Silvio WaschinaInstitute for Human Nutrition and Food Science, Division Nutriinformatics, Christian-Albrechts-University of Kiel, Kiel, Germany.
Susanne KaserDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Konrad AdenInstitute of Clinical Molecular Biology, Christian-Albrechts-University and University Hospital Schleswig-Holstein, Kiel, Germany.
Zlatko TrajanoskiBiocenter, Institute of Bioinformatics, Medical University of Innsbruck, Innsbruck, Austria.
Herbert TilgDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.
Maria EffenbergerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence supports a bidirectional gut-pancreas axis in which microbial dysbiosis, barrier dysfunction, and altered metabolite fluxes contribute to pancreatogenic diabetes (T3cDM). Whether gut microbial changes reflect systemic metabolic disturbances or primarily arise from exocrine pancreatic insufficiency (EPI) remains unclear. We profiled the gut microbiome of 48 outpatients with T3cDM, type 1 diabetes (T1DM), and healthy controls. Genus-level 16S rRNA data were analyzed using cross-validated LASSO logistic regression and patient-specific community metabolic models. T3cDM showed reduced α-diversity and distinct β-diversity compared with T1DM and controls. Key compositional shifts included enrichment of

Indexed as

Diabetes Mellitus, Type 1DysbiosisExocrine Pancreatic InsufficiencyGastrointestinal MicrobiomeAdultCase-Control StudiesFemaleHumansMaleRNA, Ribosomal, 16SRNA, Ribosomal, 16SdiabetesEPIgut microbiomemetabolomeT3cDM

Identifiers

PMID41970986
PMCPMC13065728

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.