Platelet‐derived lipids promote insulin secretion of pancreatic β cells

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 sy...

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Main Authors: Till Karwen, Katarzyna Kolczynska‐Matysiak, Carina Gross, Mona C Löffler, Mike Friedrich, Angel Loza‐Valdes, Werner Schmitz, Magdalena Wit, Filip Dziaczkowski, Andrei Belykh, Jonathan Trujillo‐Viera, Rabih El‐Merahbi, Carsten Deppermann, Sameena Nawaz, Benoit Hastoy, Agnieszka Demczuk, Manuela Erk, Mariusz R Wieckowski, Patrik Rorsman, Katrin G Heinze, David Stegner, Bernhard Nieswandt, Grzegorz Sumara
Format: Article
Language:English
Published: Springer Nature 2023-07-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.202216858
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author Till Karwen
Katarzyna Kolczynska‐Matysiak
Carina Gross
Mona C Löffler
Mike Friedrich
Angel Loza‐Valdes
Werner Schmitz
Magdalena Wit
Filip Dziaczkowski
Andrei Belykh
Jonathan Trujillo‐Viera
Rabih El‐Merahbi
Carsten Deppermann
Sameena Nawaz
Benoit Hastoy
Agnieszka Demczuk
Manuela Erk
Mariusz R Wieckowski
Patrik Rorsman
Katrin G Heinze
David Stegner
Bernhard Nieswandt
Grzegorz Sumara
author_facet Till Karwen
Katarzyna Kolczynska‐Matysiak
Carina Gross
Mona C Löffler
Mike Friedrich
Angel Loza‐Valdes
Werner Schmitz
Magdalena Wit
Filip Dziaczkowski
Andrei Belykh
Jonathan Trujillo‐Viera
Rabih El‐Merahbi
Carsten Deppermann
Sameena Nawaz
Benoit Hastoy
Agnieszka Demczuk
Manuela Erk
Mariusz R Wieckowski
Patrik Rorsman
Katrin G Heinze
David Stegner
Bernhard Nieswandt
Grzegorz Sumara
author_sort Till Karwen
collection DOAJ
description 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.
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spelling doaj-art-974cd37e10194d4682e8df439ae20f8d2024-11-10T12:37:47ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842023-07-0115912310.15252/emmm.202216858Platelet‐derived lipids promote insulin secretion of pancreatic β cellsTill Karwen0Katarzyna Kolczynska‐Matysiak1Carina Gross2Mona C Löffler3Mike Friedrich4Angel Loza‐Valdes5Werner Schmitz6Magdalena Wit7Filip Dziaczkowski8Andrei Belykh9Jonathan Trujillo‐Viera10Rabih El‐Merahbi11Carsten Deppermann12Sameena Nawaz13Benoit Hastoy14Agnieszka Demczuk15Manuela Erk16Mariusz R Wieckowski17Patrik Rorsman18Katrin G Heinze19David Stegner20Bernhard Nieswandt21Grzegorz Sumara22Rudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgNencki Institute of Experimental Biology, Polish Academy of SciencesInstitute of Experimental Biomedicine I, University Hospital WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgNencki Institute of Experimental Biology, Polish Academy of SciencesTheodor Boveri Institute, Biocenter, University of WürzburgNencki Institute of Experimental Biology, Polish Academy of SciencesNencki Institute of Experimental Biology, Polish Academy of SciencesNencki Institute of Experimental Biology, Polish Academy of SciencesRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill HospitalRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill HospitalNencki Institute of Experimental Biology, Polish Academy of SciencesRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgNencki Institute of Experimental Biology, Polish Academy of SciencesRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill HospitalRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgRudolf Virchow Center for Integrative and Translational Bioimaging, Julius‐Maximilians University of WürzburgAbstract 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.https://doi.org/10.15252/emmm.20221685820‐HETEdiabetesinsulin secretionplateletβ cell
spellingShingle Till Karwen
Katarzyna Kolczynska‐Matysiak
Carina Gross
Mona C Löffler
Mike Friedrich
Angel Loza‐Valdes
Werner Schmitz
Magdalena Wit
Filip Dziaczkowski
Andrei Belykh
Jonathan Trujillo‐Viera
Rabih El‐Merahbi
Carsten Deppermann
Sameena Nawaz
Benoit Hastoy
Agnieszka Demczuk
Manuela Erk
Mariusz R Wieckowski
Patrik Rorsman
Katrin G Heinze
David Stegner
Bernhard Nieswandt
Grzegorz Sumara
Platelet‐derived lipids promote insulin secretion of pancreatic β cells
EMBO Molecular Medicine
20‐HETE
diabetes
insulin secretion
platelet
β cell
title Platelet‐derived lipids promote insulin secretion of pancreatic β cells
title_full Platelet‐derived lipids promote insulin secretion of pancreatic β cells
title_fullStr Platelet‐derived lipids promote insulin secretion of pancreatic β cells
title_full_unstemmed Platelet‐derived lipids promote insulin secretion of pancreatic β cells
title_short Platelet‐derived lipids promote insulin secretion of pancreatic β cells
title_sort platelet derived lipids promote insulin secretion of pancreatic β cells
topic 20‐HETE
diabetes
insulin secretion
platelet
β cell
url https://doi.org/10.15252/emmm.202216858
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