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Ruiz Ojeda, F.J. ; Wang, J. ; Bäcker, T. ; Krueger, M.* ; Zamani, S. ; Rosowski, S. ; Gruber, T. ; Onogi, Y. ; Feuchtinger, A. ; Schulz, T.J.* ; Fässler, R.* ; Müller, T.D. ; García-Cáceres, C. ; Meier, M. ; Blüher, M. ; Ussar, S.

Active integrins regulate white adipose tissue insulin sensitivity and brown fat thermogenesis.

Mol. Metab. 45:101147 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Objective: Reorganization of the extracellular matrix is a prerequisite for healthy adipose tissue expansion, whereas fibrosis is a key feature of adipose dysfunction and inflammation. However, very little is known about the direct effects of impaired cell–matrix interaction in adipocyte function and insulin sensitivity. The objective of this study was to determine whether integrin activity can regulate insulin sensitivity in adipocytes and thereby systemic metabolism. Methods: We characterized integrin activity in adipose tissue and its consequences on whole-body metabolism using adipose-selective deletion of β1 integrin (Itgb1adipo-cre) and Kindlin-2 (Kind2adipo-cre) in mice. Results: We demonstrate that integrin signaling regulates white adipocyte insulin action and systemic metabolism. Consequently, loss of adipose integrin activity, similar to loss of adipose insulin receptors, results in a lipodystrophy-like phenotype and systemic insulin resistance. However, brown adipose tissue of Kind2adipo-cre and Itgb1adipo-cre mice is chronically hyperactivated and has increased substrate delivery, reduced endothelial basement membrane thickness, and increased endothelial vesicular transport. Conclusions: Thus, we establish integrin-extracellular matrix interactions as key regulators of white and brown adipose tissue function and whole-body metabolism.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adipose Tissue ; Brown Fat ; Insulin Receptor ; Insulin Resistance ; Integrins ; Kindlin-2 ; Lipodystrophy ; Obesity
Sprache englisch
Veröffentlichungsjahr 2021
HGF-Berichtsjahr 2021
ISSN (print) / ISBN 2212-8778
e-ISSN 2212-8778
Zeitschrift Molecular Metabolism
Quellenangaben Band: 45, Heft: , Seiten: , Artikelnummer: 101147 Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Institute of Developmental Genetics (IDG)
Helmholtz Pioneer Campus (HPC)
CF Pathology & Tissue Analytics (CF-PTA)
Research Unit Analytical Pathology (AAP)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
30204 - Cell Programming and Repair
30505 - New Technologies for Biomedical Discoveries
30205 - Bioengineering and Digital Health
90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
Genetics and Epidemiology
Pioneer Campus
Enabling and Novel Technologies
PSP-Element(e) G-502296-001
G-502200-001
G-500591-001
G-500500-001
G-510002-001
A-630600-001
G-500390-001
G-501900-224
G-506501-001
Förderungen European Research Council ERC
Deutsche Forschungsgemeinschaft
Fundación Alfonso Martín Escudero
DOI 10.1016/j.molmet.2020.101147
WOS ID WOS:000631823500007
Scopus ID 85099230812
PubMed ID 33359386
Erfassungsdatum 2021-03-26
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