scholarly journals Pancreatic β-cell identity in diabetes

2016 ◽  
Vol 18 ◽  
pp. 110-116 ◽  
Author(s):  
M. S. Remedi ◽  
C. Emfinger

2011 ◽  
Vol 20 (4) ◽  
pp. 419-429 ◽  
Author(s):  
Sangeeta Dhawan ◽  
Senta Georgia ◽  
Shuen-ing Tschen ◽  
Guoping Fan ◽  
Anil Bhushan


Cell Reports ◽  
2019 ◽  
Vol 26 (3) ◽  
pp. 788-801.e6 ◽  
Author(s):  
Nathan Lawlor ◽  
Eladio J. Márquez ◽  
Peter Orchard ◽  
Narisu Narisu ◽  
Muhammad Saad Shamim ◽  
...  


Author(s):  
Keisuke Kitakaze ◽  
Miho Oyadomari ◽  
Jun Zhang ◽  
Yoshimasa Hamada ◽  
Yasuhiro Takenouchi ◽  
...  


2021 ◽  
pp. 101334
Author(s):  
Nirav Florian Chhabra ◽  
Anna-Lena Amend ◽  
Aimée Bastidas-Ponce ◽  
Sibylle Sabrautzki ◽  
Marta Tarquis-Medina ◽  
...  


2020 ◽  
Author(s):  
Frédérik Oger ◽  
Cyril Bourouh ◽  
Xavier Gromada ◽  
Maeva Moreno ◽  
Charlène Carney ◽  
...  

AbstractThe loss of pancreatic β-cell identity emerges as an important feature of type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore the cell-autonomous role of the cell cycle regulator and transcription factor E2F1 in the maintenance of β-cell identity and insulin secretion. We show that the β-cell-specific loss of E2f1 function in mice triggers glucose intolerance associated with defective insulin secretion, an altered α-to-β-cell ratio, a downregulation of many β-cell genes and a concomitant increase of non-β-cell markers. Mechanistically, the epigenomic profiling of non-beta cell upregulated gene promoters identified an enrichment of bivalent H3K4me3/H3K27me3 or H3K27me3 marks. Conversely, downregulated genes were enriched in active chromatin H3K4me3 and H3K27ac histone marks. We find that histone deacetylase inhibitors modulate E2F1 transcriptional and epigenomic signatures associated with these β-cell dysfunctions. Finally, the pharmacological inhibition of E2F transcriptional activity in human islets also impairs insulin secretion and the expression of β-cell identity genes. Our data suggest that E2F1 is critical for maintaining β-cell identity through a sustained repression of non β-cell transcriptional programs.



2014 ◽  
Vol 28 (11) ◽  
pp. 4972-4985 ◽  
Author(s):  
Marina Kone ◽  
Timothy J. Pullen ◽  
Gao Sun ◽  
Mark Ibberson ◽  
Aida Martinez‐Sanchez ◽  
...  


2017 ◽  
Vol 292 (21) ◽  
pp. 8892-8906 ◽  
Author(s):  
Ryan K. Mitchell ◽  
Marie-Sophie Nguyen-Tu ◽  
Pauline Chabosseau ◽  
Rebecca M. Callingham ◽  
Timothy J. Pullen ◽  
...  


2016 ◽  
Vol 127 (1) ◽  
pp. 244-259 ◽  
Author(s):  
Giselle Domínguez Gutiérrez ◽  
Aaron S. Bender ◽  
Vincenzo Cirulli ◽  
Teresa L. Mastracci ◽  
Stephen M. Kelly ◽  
...  


2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.



Sign in / Sign up

Export Citation Format

Share Document