PuSH - Publikationsserver des Helmholtz Zentrums München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Cohrs, C.M. ; Panzer, J.K. ; Drotar, D.M. ; Enos, S.J. ; Kipke, N. ; Chen, C. ; Schöniger, E. ; Ehehalt, F.* ; Distler, M.* ; Brennand, A.* ; Bornstein, S.R. ; Weitz, J. ; Solimena, M. ; Speier, S.

Dysfunction of persisting β cells is a key feature of early type 2 diabetes pathogenesis.

Cell Rep. 31:107469 (2020)
Postprint Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
Type 2 diabetes is characterized by peripheral insulin resistance and insufficient insulin release from pancreatic islet beta cells. However, the role and sequence of b cell dysfunction and mass loss for reduced insulin levels in type 2 diabetes pathogenesis are unclear. Here, we exploit freshly explanted pancreas specimens from metabolically phenotyped surgical patients using an in situ tissue slice technology. This approach allows assessment of beta cell volume and function within pancreas samples of metabolically stratified individuals. We show that, in tissue of pre-diabetic, impaired glucose-tolerant subjects, beta cell volume is unchanged, but function significantly deteriorates, exhibiting increased basal release and loss of first-phase insulin secretion. In individuals with type 2 diabetes, function within the sustained beta cell volume further declines. These results indicate that dysfunction of persisting beta cells is a key factor in the early development and progression of type 2 diabetes, representing a major target for diabetes prevention and therapy.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
8.109
1.707
33
48
Tags
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern

Zusatzinfos bearbeiten
Eigene Tags bearbeiten
Privat
Eigene Anmerkung bearbeiten
Privat
Auf Publikationslisten für
Homepage nicht anzeigen
Als besondere Publikation
markieren
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Beta Cell Function ; Beta Cell Mass ; Human Pancreas ; Insulin Secretion ; Type 2 Diabetes; Impaired Glucose-tolerance; Insulin-resistance; In-situ; Mass; Islet; Mechanisms; Pancreas; Risk; Secretion; Turnover
Sprache englisch
Veröffentlichungsjahr 2020
HGF-Berichtsjahr 2020
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 31, Heft: 1, Seiten: , Artikelnummer: 107469 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-005
G-502600-001
DOI 10.1016/j.celrep.2020.03.033
WOS ID WOS:000524976500006
Scopus ID 85082749972
Erfassungsdatum 2020-05-04
[➜Korrektur melden]