scholarly journals Beta-cell destruction and preservation in childhood and adult onset type 1 diabetes

Endocrine ◽  
2015 ◽  
Vol 49 (3) ◽  
pp. 693-702 ◽  
Author(s):  
Ananta Poudel ◽  
Omid Savari ◽  
Deborah A. Striegel ◽  
Vipul Periwal ◽  
Jerome Taxy ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Adult Onset ◽  
Onset Type ◽  
Beta Cell Destruction ◽  
Cell Destruction

scholarly journals Islet–immune interactions in type 1 diabetes: the nexus of beta cell destruction

2019 ◽  
Vol 198 (3) ◽  
pp. 326-340 ◽  
Author(s):  
L. Peters ◽  
A. Posgai ◽  
T. M. Brusko
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Beta Cell Destruction ◽  
Cell Destruction

scholarly journals Islet-Specific CTL Cloned from a Type 1 Diabetes Patient Cause Beta-Cell Destruction after Engraftment into HLA-A2 Transgenic NOD/SCID/IL2RG Null Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49213 ◽  
Author(s):  
Wendy W. J. Unger ◽  
Todd Pearson ◽  
Joana R. F. Abreu ◽  
Sandra Laban ◽  
Arno R. van der Slik ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Diabetes Patient ◽  
Beta Cell Destruction ◽  
Cell Destruction

scholarly journals Is the process of beta-cell destruction in type 1 diabetes at time of diagnosis more extensive in females than in males?

2001 ◽  
pp. 757-761 ◽  
Author(s):  
P Pozzilli ◽  
CA Mesturino ◽  
A Crino ◽  
TM Gross ◽  
LM Jeng ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Insulin Therapy ◽  
Metabolic Control ◽  
Metabolic Parameters ◽  
C Peptide ◽  
Beta Cell Destruction ◽  
Cell Destruction ◽  
Good Metabolic Control

OBJECTIVE: To evaluate sex differences in patients with insulin-dependent diabetes mellitus (type 1 diabetes) by comparing the integrated parameters of metabolic control at the time of clinical diagnosis and 3 months after intensive insulin therapy in pre-pubertal, pubertal and post-pubertal patients. DESIGN: A total of 331 consecutive patients with newly diagnosed type 1 diabetes were studied. The mean age of the group was 15 years (s.d. 8.1; range 5-23 years). Patients were stratified into three groups according to their age at disease onset: pre-pubertal (ages 5-9 years), pubertal (ages 10-18 years) and post-pubertal (ages 19-23 years). METHODS: Glycated haemoglobin (HbA(1c)), insulin dose and both basal and glucagon-stimulated C-peptide were evaluated at diagnosis and after 3 months of insulin therapy. RESULTS: We found that females diagnosed after puberty were those with the lowest basal C-peptide compared with males (P=0.005). No statistically significant differences were observed for other metabolic parameters. When the entire group was evaluated, females at the time of diagnosis showed significant lower body mass index (P=0.001), lower basal C-peptide (P=0.021) and higher HbA(1c) (P=0.023) and required more insulin than males (P<0.001). After 3 months of therapy, only a significantly greater dose of insulin was observed in females compared with males (P=0.001), with similar good metabolic control as assessed by HbA(1c). CONCLUSIONS: We conclude that the process of beta-cell destruction at diagnosis may be more extensive in post-pubertal females than in males. Moreover, after the introduction of insulin therapy, females and males show similar metabolic parameters, although females still require significantly more insulin than males to achieve good metabolic control, 3 months after diagnosis.

scholarly journals Endoplasmic Reticulum-Mitochondria Crosstalk and Beta-Cell Destruction in Type 1 Diabetes

2021 ◽  
Vol 12 ◽  
Author(s):  
Saurabh Vig ◽  
Joost M. Lambooij ◽  
Arnaud Zaldumbide ◽  
Bruno Guigas
Keyword(s):  
Endoplasmic Reticulum ◽  
Type 1 Diabetes ◽  
Beta Cell ◽  
Beta Cells ◽  
Beta Cell Destruction ◽  
Unfolded Protein ◽  
Cell Destruction ◽  
The Unfolded Protein Response ◽  
And Function

Beta-cell destruction in type 1 diabetes (T1D) results from the combined effect of inflammation and recurrent autoimmunity. In response to inflammatory signals, beta-cells engage adaptive mechanisms where the endoplasmic reticulum (ER) and mitochondria act in concert to restore cellular homeostasis. In the recent years it has become clear that this adaptive phase may trigger the development of autoimmunity by the generation of autoantigens recognized by autoreactive CD8 T cells. The participation of the ER stress and the unfolded protein response to the increased visibility of beta-cells to the immune system has been largely described. However, the role of the other cellular organelles, and in particular the mitochondria that are central mediator for beta-cell survival and function, remains poorly investigated. In this review we will dissect the crosstalk between the ER and mitochondria in the context of T1D, highlighting the key role played by this interaction in beta-cell dysfunctions and immune activation, especially through regulation of calcium homeostasis, oxidative stress and generation of mitochondrial-derived factors.

scholarly journals Restrain of beta-cell destruction and stimulation of beta-cell regeneration in type 1 diabetes

2015 ◽  
Vol 14 (3) ◽  
pp. 35-40
Author(s):  
Leszek Szewczyk ◽  
◽  
Anna Bury ◽  
Robert Piekarski ◽  
◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Cell Regeneration ◽  
Beta Cell Regeneration ◽  
Beta Cell Destruction ◽  
Cell Destruction ◽  
Stimulation Of
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