scholarly journals The role of apoptosis in pathogenesis of type 1 diabetes mellitus

2010 ◽  
Vol 13 (1) ◽  
pp. 45-49
Author(s):  
Elena Vladimirovna Pekareva ◽  
Tatiana Vasil'evna Nikonova ◽  
Olga Mikhailovna Smirnova
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Beta Cell ◽  
Type 1 Diabetes Mellitus ◽  
Beta Cells ◽  
Cell Apoptosis ◽  
Pancreatic Beta Cells ◽  
Beta Cell Apoptosis

Type 1 diabetes mellitus (DM1) is known to be associated with progressive destruction of pancreatic beta-cells. Apoptosis plays the key role in this destructiveprocess. The paper focuses on major mechanisms underlying activation of beta-cell apoptosis and its role in regulation of immune processes inpatients with DM1.

scholarly journals Nano-curcumin safely prevents streptozotocin-induced inflammation and apoptosis in pancreatic beta cells for effective management of Type 1 diabetes mellitus

2017 ◽  
Vol 174 (13) ◽  
pp. 2074-2084 ◽  
Author(s):  
Raghu Ganugula ◽  
Meenakshi Arora ◽  
Patcharawalai Jaisamut ◽  
Ruedeekorn Wiwattanapatapee ◽  
Heather G Jørgensen ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Effective Management

Residual beta-cell function and spontaneous clinical remission in type 1 diabetes mellitus: the role of puberty

1998 ◽  
Vol 35 (2) ◽  
pp. 91-95 ◽  
Author(s):  
R. Bonfanti ◽  
E. Bognetti ◽  
F. Meschi ◽  
A. Brunelli ◽  
M. C. Riva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Beta Cell ◽  
Type 1 Diabetes Mellitus ◽  
Clinical Remission ◽  
Beta Cell Function ◽  
Cell Function

scholarly journals The miRNAs miR-211-5p and miR-204-5p modulate ER stress in human beta cells

2019 ◽  
Vol 63 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Fabio Arturo Grieco ◽  
Andrea Alex Schiavo ◽  
Flora Brozzi ◽  
Jonas Juan-Mateu ◽  
Marco Bugliani ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cell ◽  
Er Stress ◽  
Beta Cells ◽  
Cell Apoptosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Beta Cell Apoptosis ◽  
Human Beta Cells

miRNAs are a class of small non-coding RNAs that regulate gene expression. Type 1 diabetes is an autoimmune disease characterized by insulitis (islets inflammation) and pancreatic beta cell destruction. The pro-inflammatory cytokines interleukin 1 beta (IL1B) and interferon gamma (IFNG) are released during insulitis and trigger endoplasmic reticulum (ER) stress and expression of pro-apoptotic members of the BCL2 protein family in beta cells, thus contributing to their death. The nature of miRNAs that regulate ER stress and beta cell apoptosis remains to be elucidated. We have performed a global miRNA expression profile on cytokine-treated human islets and observed a marked downregulation of miR-211-5p. By real-time PCR and Western blot analysis, we confirmed cytokine-induced changes in the expression of miR-211-5p and the closely related miR-204-5p and downstream ER stress related genes in human beta cells. Blocking of endogenous miRNA-211-5p and miR-204-5p by the same inhibitor (it is not possible to block separately these two miRs) increased human beta cell apoptosis, as measured by Hoechst/propidium Iodide staining and by determination of cleaved caspase-3 activation. Interestingly, miRs-211-5p and 204-5p regulate the expression of several ER stress markers downstream of PERK, particularly the pro-apoptotic protein DDIT3 (also known as CHOP). Blocking CHOP expression by a specific siRNA partially prevented the increased apoptosis observed following miR-211-5p/miR-204-5p inhibition. These observations identify a novel crosstalk between miRNAs, ER stress and beta cell apoptosis in early type 1 diabetes.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

2016 ◽  
Vol 174 (4) ◽  
pp. R127-R138 ◽  
Author(s):  
F S Hough ◽  
D D Pierroz ◽  
C Cooper ◽  
S L Ferrari ◽  
_ _
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Bone Fragility ◽  
Mineral Density ◽  
Good Glycaemic Control ◽  
Marrow Adiposity ◽  
Igf1 Deficiency

Subjects with type 1 diabetes mellitus (T1DM) have decreased bone mineral density and an up to sixfold increase in fracture risk. Yet bone fragility is not commonly regarded as another unique complication of diabetes. Both animals with experimentally induced insulin deficiency syndromes and patients with T1DM have impaired osteoblastic bone formation, with or without increased bone resorption. Insulin/IGF1 deficiency appears to be a major pathogenetic mechanism involved, along with glucose toxicity, marrow adiposity, inflammation, adipokine and other metabolic alterations that may all play a role on altering bone turnover. In turn, increasing physical activity in children with diabetes as well as good glycaemic control appears to provide some improvement of bone parameters, although robust clinical studies are still lacking. In this context, the role of osteoporosis drugs remains unknown.

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