Evidence map›Paper›PMID 37490001›Full record

ArticleEMBO molecular medicine2023

Platelet-derived lipids promote insulin secretion of pancreatic β cells.

Till Karwen, Katarzyna Kolczynska-Matysiak, Carina Gross, Mona C Löffler, Mike Friedrich, Angel Loza-Valdes, Werner Schmitz, Magdalena Wit, Filip Dziaczkowski, Andrei Belykh and 13 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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

23 authors at 5 institutions in 4 countries.

Till Karwen *Rudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-4110-2065
Katarzyna Kolczynska-Matysiak *Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0002-8712-2996
Carina GrossInstitute of Experimental Biomedicine I, University Hospital Würzburg, Würzburg, Germany.
Mona C LöfflerRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0001-5325-8177
Mike FriedrichRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Angel Loza-ValdesNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0003-1957-4883
Werner SchmitzTheodor Boveri Institute, Biocenter, University of Würzburg, Würzburg, Germany.ORCID 0000-0003-0485-7303
Magdalena WitNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0002-0995-2732
Filip DziaczkowskiNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0003-4807-7456
Andrei BelykhNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0001-9766-2104
Jonathan Trujillo-VieraRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Rabih El-MerahbiRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Carsten DeppermannRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-3740-8635
Sameena NawazRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK.ORCID 0000-0002-3894-4600
Benoit HastoyRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK.
Agnieszka DemczukNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0001-9868-7653
Manuela ErkRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Mariusz R WieckowskiNencki Institute of Experimental Biology, Polish Academy of Sciences, Warszawa, Poland.ORCID 0000-0003-0789-4521
Patrik RorsmanRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK.
Katrin G HeinzeRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-2372-6800
David StegnerRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-1059-9865
Bernhard NieswandtRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-1454-7413
Grzegorz SumaraRudolf Virchow Center for Integrative and Translational Bioimaging, Julius-Maximilians University of Würzburg, Würzburg, Germany.ORCID 0000-0003-1502-6265
University of Würzburg · DEInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLChurchill Hospital · GBJohannes Gutenberg University Mainz · DEUniversitätsklinikum Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperreactive platelets are commonly observed in diabetic patients indicating a potential link between glucose homeostasis and platelet reactivity. This raises the possibility that platelets may play a role in the regulation of metabolism. Pancreatic β cells are the central regulators of systemic glucose homeostasis. Here, we show that factor(s) derived from β cells stimulate platelet activity and platelets selectively localize to the vascular endothelium of pancreatic islets. Both depletion of platelets and ablation of major platelet adhesion or activation pathways consistently resulted in impaired glucose tolerance and decreased circulating insulin levels. Furthermore, we found platelet-derived lipid classes to promote insulin secretion and identified 20-Hydroxyeicosatetraenoic acid (20-HETE) as the main factor promoting β cells function. Finally, we demonstrate that the levels of platelet-derived 20-HETE decline with age and that this parallels with reduced impact of platelets on β cell function. Our findings identify an unexpected function of platelets in the regulation of insulin secretion and glucose metabolism, which promotes metabolic fitness in young individuals.

Indexed as

Insulin-Secreting CellsBlood PlateletsGlucoseHumansInsulinInsulin SecretionGlucoseInsulin20-HETEdiabetesinsulin secretionplateletβ cell

Identifiers

PMID37490001
PMCPMC10493578
OpenAlexW4385230122

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.