Evidence map›Paper›PMID 40263590›Full record

ArticleMolecular systems biology2025

Metabolic modelling reveals increased autonomy and antagonism in type 2 diabetic gut microbiota.

A Samer Kadibalban, Axel Künstner, Torsten Schröder, Julius Zauleck, Oliver Witt, Georgios Marinos, Christoph Kaleta

Abstract read
In one paragraph

Article in Molecular systems biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

7 authors.

A Samer KadibalbanMedical Systems Biology Group, University Hospital Schleswig-Holstein Campus Kiel & Kiel University, Kiel, Germany.ORCID http://orcid.org/0009-0001-9726-543X
Axel KünstnerMedical Systems Biology Group, Lübeck Institute for Experimental Dermatology, University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0003-0692-2105
Torsten SchröderPerfood GmbH, Lübeck, Schleswig-Holstein, Germany.ORCID http://orcid.org/0009-0006-4897-1481
Julius ZauleckPerfood GmbH, Lübeck, Schleswig-Holstein, Germany.ORCID http://orcid.org/0009-0002-1391-5755
Oliver WittPerfood GmbH, Lübeck, Schleswig-Holstein, Germany.ORCID http://orcid.org/0009-0000-8665-9137
Georgios MarinosMedical Systems Biology Group, University Hospital Schleswig-Holstein Campus Kiel & Kiel University, Kiel, Germany.ORCID http://orcid.org/0000-0002-6443-7696
Christoph KaletaMedical Systems Biology Group, University Hospital Schleswig-Holstein Campus Kiel & Kiel University, Kiel, Germany. c.kaleta@iem.uni-kiel.de.ORCID http://orcid.org/0000-0001-8004-9514

Funding

Deutsche Forschungsgemeinschaft (DFG) EXC2167ExoMod KA 3541/20-1
6 · The paper itself

Abstract

Type 2 diabetes (T2D) presents a global health concern, with evidence highlighting the role of the human gut microbiome in metabolic diseases. This study employs metabolic modelling to elucidate changes in host-microbiome interactions in T2D. Glucose levels, diet, 16S sequences and metadata were collected for 1866 individuals. In addition, microbial community models, and ecological interactions were simulated for the gut microbiomes. Our findings revealed a significant decrease in metabolic fluxes provided by the host's diet to the microbiome in T2D patients, accompanied by increased within-community exchanges. Moreover, the diabetic microbiomes shift towards increased exploitative ecological interactions at the expense of collaborative interactions. The reduced microbiome-to-host butyrate flux, along with decreased fluxes of amino acids (including tryptophan), nucleotides, and B vitamins from the host's diet, further highlight the dysregulation in microbial-host interactions in diabetes. In addition, microbiomes of T2D patients exhibit enrichment in energy metabolism, indicative of increased metabolic activity and antagonism. This study sheds light on the increased microbiome autonomy and antagonism accompanying diabetes, and provides candidate metabolic targets for intervention studies and experimental validation.

Indexed as

Diabetes Mellitus, Type 2Gastrointestinal MicrobiomeButyratesDietEnergy MetabolismFemaleHost Microbial InteractionsHumansMaleMiddle AgedModels, BiologicalButyratesDiabetesGut Microbial CommunityMetabolic ModellingMicrobiomeT2D

Identifiers

PMID40263590
PMCPMC12130202

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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.