Evidence map›Paper›PMID 42459661›Full record

ArticleFrontiers in immunology2026

Reduced platelet count in mice protects against glucose intolerance and beta cell loss during a long-term high-fat diet.

Niklas Burkhard, Johannes Hoch, Shanshan Zhang, Muataz Ali Hamad, Nicolas Schommer, Carolin Mogler, Daniela Stallmann, Pierre Mangin, Krystin Krauel, Daniel Duerschmied and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Niklas BurkhardCardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Johannes HochCardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Shanshan ZhangCardiology, Haemostaseology, and Medical Intensive Care, Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Muataz Ali HamadCardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Nicolas SchommerCardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Carolin MoglerInstitute of Pathology, School of Medicine and Health, Technical University Munich, Munich, Germany.
Daniela StallmannCardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Pierre ManginUniversité de Strasbourg, Institut National de la Santé et de la Recherche Médicale, Etablissement Français du Sang Grand-Est, Unité Mixte de Recherche-S1255, Fédération de Medecine Translationnelle de Strasbourg, Strasbourg, France.
Krystin KrauelCardiology, Haemostaseology, and Medical Intensive Care, Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Daniel Duerschmied *Cardiology, Haemostaseology, and Medical Intensive Care, Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Nancy Schanze *Cardiology and Angiology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Platelets promote hemostasis and modulate different inflammatory and immunological processes. Recently, it was reported that platelets interact with pancreatic beta cells to increase insulin secretion. Inflammatory conditions and a lack of sufficient insulin secretion drive the pathogenesis of type 2 diabetes (T2D) in the context of obesity. However, the specific role of platelets during the development of obesity-related T2D has not yet been investigated. Methods: Thrombopoietin receptor knockout ( Results: After HFD feeding, obese Discussion: These results suggests that thrombocytopenia protects pancreatic beta cells in an obesity mouse model of T2D, thereby preserving insulin secretion and improving glucose tolerance.

Indexed as

Blood PlateletsDiet, High-FatGlucose IntoleranceInsulin-Secreting CellsThrombocytopeniaAnimalsDiabetes Mellitus, Type 2InsulinInsulin ResistanceMaleMiceMice, Inbred C57BLMice, KnockoutObesityPlatelet CountReceptors, ThrombopoietinInsulinMpl protein, mouseReceptors, Thrombopoietindiabetesglucose toleranceinsulin secretionobesitypancreatic beta cellsplateletsthrombocytopenia

Identifiers

PMID42459661
PMCPMC13368534

What Socratic 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 Socratic graph.