Evidence map›Paper›PMID 41393294›Full record

ArticleFrontiers in endocrinology2025

Antibiotic-induced gut microbiota depletion enhances glucose tolerance linked to GLP-1 signaling.

Alexandra Kellenberger, Revati Sumukh Dewal, Alice de Wouters d'Oplinter, Andreas Sichert, Markus Heine, Marceline M Fuh, Emma Slack, Tenagne Delessa Challa, Christian Wolfrum

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2025. 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. Review
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

9 authors.

Alexandra KellenbergerLaboratory of Translational Nutrition Biology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.
Revati Sumukh DewalLaboratory of Translational Nutrition Biology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.
Alice de Wouters d'OplinterLaboratory for Mucosal Immunology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Zurich, Switzerland.
Andreas SichertLaboratory for Mucosal Immunology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Zurich, Switzerland.
Markus HeineDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Marceline M FuhDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Emma SlackLaboratory for Mucosal Immunology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Zurich, Switzerland.
Tenagne Delessa ChallaLaboratory of Translational Nutrition Biology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.
Christian WolfrumLaboratory of Translational Nutrition Biology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Depletion of the gut microbiota is known to improve glucose metabolism and modify thermogenic capacity in mice. However, the underlying mechanisms remain unclear. In this study, we aimed to determine whether the browning effect observed after antibiotic treatment contributes to metabolic modifications and to investigate the potential central role of GLP-1 in enhancing glucose metabolism. Methods: Using an inducible Ucp1DTR mouse model to transiently ablate UCP1 Results: We demonstrate that gut microbiota depletion improved glucose tolerance independent of UCP1 Discussion: Our findings suggest that the metabolic improvements following gut microbiota depletion are primarily driven by GLP-1 signaling, rather than UCP1⁺ cell activation. These results highlight the complex interplay between the gut microbiome and metabolic health, offering insights into potential therapeutic targets for improving glucose metabolism through modulation of basal GLP-1 signaling.

Indexed as

Anti-Bacterial AgentsGastrointestinal MicrobiomeAnimalsBile Acids and SaltsGlucagon-Like Peptide-1 ReceptorGlucose IntoleranceMiceMice, KnockoutAnti-Bacterial AgentsBile Acids and SaltsGlucagon-Like Peptide-1 Receptorantibiotic treatmentbile acidsGLP-1 signalingglucose tolerancegut microbiomegut microbiota depletioninsulin sensitivityUCP1-independent mechanism

Identifiers

PMID41393294
PMCPMC12695531

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.