Identification of Key β Cell Gene Signaling Pathways Involved in Type 1 Diabetes

2004 ◽  
Vol 1037 (1) ◽  
pp. 203-207 ◽  
Author(s):  
DIEGO SILVA ◽  
NIKOLAI PETROVSKY
Keyword(s):  
Type 1 Diabetes ◽  
Signaling Pathways ◽  
Β Cell ◽  
Cell Gene

scholarly journals From Pancreatic β-Cell Gene Networks to Novel Therapies for Type 1 Diabetes

Diabetes ◽  
2021 ◽  
Vol 70 (9) ◽  
pp. 1915-1925 ◽  
Author(s):  
Decio L. Eizirik ◽  
Florian Szymczak ◽  
Maria Inês Alvelos ◽  
Frank Martin
Keyword(s):  
Type 1 Diabetes ◽  
Gene Networks ◽  
Novel Therapies ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Gene

scholarly journals One repeated transplantation of allogeneic umbilical cord mesenchymal stromal cells in type 1 diabetes: an open parallel controlled clinical study

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jing Lu ◽  
Shan-mei Shen ◽  
Qing Ling ◽  
Bin Wang ◽  
Li-rong Li ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Stromal Cells ◽  
Treated Group ◽  
Control Group ◽  
Adult Onset ◽  
Β Cell ◽  
Juvenile Onset ◽  
C Peptide

Abstract Background The preservation or restoration of β cell function in type 1 diabetes (T1D) remains as an attractive and challengeable therapeutic target. Mesenchymal stromal cells (MSCs) are multipotent cells with high capacity of immunoregulation, which emerged as a promising cell-based therapy for many immune disorders. The objective of this study was to examine the efficacy and safety of one repeated transplantation of allogeneic MSCs in individuals with T1D. Methods This was a nonrandomized, open-label, parallel-armed prospective study. MSCs were isolated from umbilical cord (UC) of healthy donors. Fifty-three participants including 33 adult-onset (≥ 18 years) and 20 juvenile-onset T1D were enrolled. Twenty-seven subjects (MSC-treated group) received an initial systemic infusion of allogeneic UC-MSCs, followed by a repeat course at 3 months, whereas the control group (n = 26) only received standard care based on intensive insulin therapy. Data at 1-year follow-up was reported in this study. The primary endpoint was clinical remission defined as a 10% increase from baseline in the level of fasting and/or postprandial C-peptide. The secondary endpoints included side effects, serum levels of HbA1c, changes in fasting and postprandial C-peptide, and daily insulin doses. Results After 1-year follow-up, 40.7% subjects in MSC-treated group achieved the primary endpoint, significantly higher than that in the control arm. Three subjects in MSC-treated group, in contrast to none in control group, achieved insulin independence and maintained insulin free for 3 to 12 months. Among the adult-onset T1D, the percent change of postprandial C-peptide was significantly increased in MSC-treated group than in the control group. However, changes in fasting or postprandial C-peptide were not significantly different between groups among the juvenile-onset T1D. Multivariable logistic regression assay indicated that lower fasting C-peptide and higher dose of UC-MSC correlated with achievement of clinical remission after transplantation. No severe side effects were observed. Conclusion One repeated intravenous dose of allogeneic UC-MSCs is safe in people with recent-onset T1D and may result in better islet β cell preservation during the first year after diagnosis compared to standard treatment alone. Trial registration ChiCTR2100045434. Registered on April 15, 2021—retrospectively registered, http://www.chictr.org.cn/

scholarly journals β Cell death and dysfunction during type 1 diabetes development in at-risk individuals

2015 ◽  
Vol 125 (3) ◽  
pp. 1163-1173 ◽  
Author(s):  
Kevan C. Herold ◽  
Sahar Usmani-Brown ◽  
Tara Ghazi ◽  
Jasmin Lebastchi ◽  
Craig A. Beam ◽  
...  
Keyword(s):  
At Risk ◽  
Cell Death ◽  
Type 1 Diabetes ◽  
Β Cell ◽  
Diabetes Development

Brown alga Ecklonia cava attenuates type 1 diabetes by activating AMPK and Akt signaling pathways

2010 ◽  
Vol 48 (2) ◽  
pp. 509-516 ◽  
Author(s):  
Changkeun Kang ◽  
Yeung Bae Jin ◽  
Hyunkyoung Lee ◽  
Mijin Cha ◽  
Eun-tae Sohn ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Signaling Pathways ◽  
Brown Alga ◽  
Akt Signaling ◽  
Ecklonia Cava

Association of T-cell reactivity with β-cell function in recent onset type 1 diabetes patients

2010 ◽  
Vol 34 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Christian Pfleger ◽  
Guido Meierhoff ◽  
Hubert Kolb ◽  
Nanette C. Schloot
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Cell Function ◽  
Β Cell ◽  
Cell Reactivity ◽  
Recent Onset ◽  
Onset Type ◽  
Β Cell Function ◽  
T Cell Reactivity

scholarly journals The challenge of modulating β-cell autoimmunity in type 1 diabetes

2019 ◽  
Vol 7 (1) ◽  
pp. 52-64 ◽  
Author(s):  
Mark A Atkinson ◽  
Bart O Roep ◽  
Amanda Posgai ◽  
Daniel C S Wheeler ◽  
Mark Peakman
Keyword(s):  
Type 1 Diabetes ◽  
Β Cell

Use of a systems biology approach to understand pancreatic β-cell death in Type 1 diabetes

2008 ◽  
Vol 36 (3) ◽  
pp. 321-327 ◽  
Author(s):  
Decio L. Eizirik ◽  
Fabrice Moore ◽  
Daisy Flamez ◽  
Fernanda Ortis
Keyword(s):  
Cell Death ◽  
Type 1 Diabetes ◽  
Systems Biology ◽  
Gene Networks ◽  
Nuclear Factor Κb ◽  
Signal Transducer ◽  
Trial And Error ◽  
Β Cells ◽  
Β Cell

Accumulating evidence indicates that β-cells die by apoptosis in T1DM (Type 1 diabetes mellitus). Apoptosis is an active gene-directed process, and recent observations suggest that β-cell apoptosis depends on the parallel and/or sequential up- and down-regulation of hundreds of genes controlled by key transcription factors such as NF-κB (nuclear factor κB) and STAT-1 (signal transducer and activator of transcription 1). Understanding the regulation of these gene networks, and how they modulate β-cell death and the ‘dialogue’ between β-cells and the immune system, will require a systems biology approach to the problem. This will hopefully allow the search for a cure for T1DM to move from a ‘trial-and-error’ approach to one that is really mechanistically driven.

scholarly journals Autoreactive T effector memory differentiation mirrors β cell function in type 1 diabetes

2018 ◽  
Vol 128 (8) ◽  
pp. 3460-3474 ◽  
Author(s):  
Lorraine Yeo ◽  
Alyssa Woodwyk ◽  
Sanjana Sood ◽  
Anna Lorenc ◽  
Martin Eichmann ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Cell Function ◽  
Effector Memory ◽  
Β Cell ◽  
Β Cell Function ◽  
Memory Differentiation
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