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Kulaj, K. ; Harger, A. ; Bauer, M. ; Caliskan, Ö.S. ; Gupta, T.K.* ; Chiang, D.M.* ; Milbank, E. ; Reber, J. ; Karlas, A. ; Kotzbeck, P. ; Sailer, D.N. ; Volta, F. ; Lutter, D. ; Prakash, S. ; Merl-Pham, J. ; Ntziachristos, V. ; Hauner, H.* ; Pfaffl, M.W.* ; Tschöp, M.H. ; Müller, T.D. ; Hauck, S.M. ; Engel, B.D. ; Gerdes, J.M. ; Pfluger, P.T. ; Krahmer, N. ; Stemmer, K.

Adipocyte-derived extracellular vesicles increase insulin secretion through transport of insulinotropic protein cargo.

Nat. Commun. 14:709 (2023)
Postprint DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Adipocyte-derived extracellular vesicles (AdEVs) are membranous nanoparticles that convey communication from adipose tissue to other organs. Here, to delineate their role as messengers with glucoregulatory nature, we paired fluorescence AdEV-tracing and SILAC-labeling with (phospho)proteomics, and revealed that AdEVs transfer functional insulinotropic protein cargo into pancreatic β-cells. Upon transfer, AdEV proteins were subjects for phosphorylation, augmented insulinotropic GPCR/cAMP/PKA signaling by increasing total protein abundances and phosphosite dynamics, and ultimately enhanced 1st-phase glucose-stimulated insulin secretion (GSIS) in murine islets. Notably, insulinotropic effects were restricted to AdEVs isolated from obese and insulin resistant, but not lean mice, which was consistent with differential protein loads and AdEV luminal morphologies. Likewise, in vivo pre-treatment with AdEVs from obese but not lean mice amplified insulin secretion and glucose tolerance in mice. This data suggests that secreted AdEVs can inform pancreatic β-cells about insulin resistance in adipose tissue in order to amplify GSIS in times of increased insulin demand.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Skeletal-muscle; Adipose-tissue; Obesity; Expression; Inflammation; Resistance; Receptor; Mirnas
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 14, Heft: 1, Seiten: , Artikelnummer: 709 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Institute of Biological and Medical Imaging (IBMI)
Institute of Diabetes and Regeneration Research (IDR)
CF Metabolomics & Proteomics (CF-MPC)
Helmholtz Pioneer Campus (HPC)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
30205 - Bioengineering and Digital Health
30203 - Molecular Targets and Therapies
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
Pioneer Campus
PSP-Element(e) G-501900-221
G-502200-001
G-502200-009
G-505500-001
G-505593-001
G-501900-233
G-502297-001
G-505700-001
G-510008-001
G-502294-001
A-630700-001
Förderungen Helmholtz Zentrum Munchen (Helmholtz Developmental Project Grant)
German Research Foundation (DFG)
DFG
German Research Foundation
European Research Council (ERC, CoG Trusted)
Helmholtz-Israel-Cooperation in Personalized Medicine
European Research Council (ERC, CoG Yoyo-LepReSens)
Helmholtz Zentrum Munchen (Helmholtz Portfolio Grant)
Else Kroner-Fresenius-Foundation
ERC (AdG HypoFlam)
Alexander von Humboldt Foundation
Helmholtz Alliance ICEMED by Helmholtz Association
Helmholtz Initiative on Personalized Medicine iMed by Helmholtz Association
Helmholtz cross-program topic "Metabolic Dysfunction"
University of Augsburg

European Research Council (ERC, PREMSOT)
DOI 10.1038/s41467-023-36148-1
WOS ID 001023549000010
Scopus ID 85147784672
PubMed ID 36759608
Erfassungsdatum 2023-02-17
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