scholarly journals MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes

2014 ◽  
Vol 20 (4) ◽  
pp. 385-397 ◽  
Author(s):  
Amin Ardestani ◽  
Federico Paroni ◽  
Zahra Azizi ◽  
Supreet Kaur ◽  
Vrushali Khobragade ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Apoptosis ◽  
Beta Cell Apoptosis

GDF15 Is Induced by T1D-Associated Cytokines and ER Stress and Promotes Beta-Cell Apoptosis

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2109-P ◽  
Author(s):  
GUANLAN XU ◽  
LANCE THIELEN ◽  
JUNQIN CHEN ◽  
SEONGHO JO ◽  
ANATH SHALEV
Keyword(s):  
Beta Cell ◽  
Er Stress ◽  
Cell Apoptosis ◽  
Beta Cell Apoptosis

Ruthenium complexes as inhibitors of human islet amyloid polypeptide aggregation, an effect that prevents beta cell apoptosis

RSC Advances ◽  
2015 ◽  
Vol 5 (23) ◽  
pp. 17405-17412 ◽  
Author(s):  
Lijuan Ma ◽  
Yuanting Fu ◽  
Lianling Yu ◽  
Xiaoling Li ◽  
Wenjie Zheng ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Apoptosis ◽  
Cell Damage ◽  
Islet Amyloid Polypeptide ◽  
Ruthenium Complexes ◽  
Human Islet ◽  
Ros Generation ◽  
Beta Cell Apoptosis ◽  
Islet Amyloid ◽  
Application Potential

Herein we show that ruthenium complexes could inhibit fibrosis of hIAPP and protect the hIAPP-induced cell damage by suppressing ROS generation, indicating the application potential of the complexes in treatment of T2DM by targeting hIAPP.

Imidazoline compounds protect against interleukin 1beta-induced beta-cell apoptosis

Diabetes ◽  
2001 ◽  
Vol 50 (Supplement 1) ◽  
pp. S70-S76 ◽  
Author(s):  
S. V. Zaitsev ◽  
I. B. Appelskog ◽  
I. L. Kapelioukh ◽  
S. Yang ◽  
M. K hler ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Apoptosis ◽  
Beta Cell Apoptosis ◽  
Interleukin 1Beta ◽  
Imidazoline Compounds

scholarly journals Oxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis

Diabetologia ◽  
2009 ◽  
Vol 52 (4) ◽  
pp. 626-635 ◽  
Author(s):  
S. Zraika ◽  
R. L. Hull ◽  
J. Udayasankar ◽  
K. Aston-Mourney ◽  
S. L. Subramanian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Cell Apoptosis ◽  
Beta Cell Apoptosis ◽  
Amyloid Formation ◽  
Islet Amyloid

scholarly journals Bergenin protects pancreatic beta cells against cytokine-induced apoptosis in INS-1E cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0241349
Author(s):  
Sajid Ali Rajput ◽  
Munazza Raza Mirza ◽  
M. Iqbal Choudhary
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cells ◽  
Proinflammatory Cytokines ◽  
Cell Apoptosis ◽  
Pancreatic Beta Cells ◽  
Cell Function ◽  
Beta Cell Apoptosis ◽  
Atp Levels ◽  
Induced Apoptosis

Beta cell apoptosis induced by proinflammatory cytokines is one of the hallmarks of diabetes. Small molecules which can inhibit the cytokine-induced apoptosis could lead to new drug candidates that can be used in combination with existing therapeutic interventions against diabetes. The current study evaluated several effects of bergenin, an isocoumarin derivative, in beta cells in the presence of cytokines. These included (i) increase in beta cell viability (by measuring cellular ATP levels) (ii) suppression of beta cell apoptosis (by measuring caspase activity), (iii) improvement in beta cell function (by measuring glucose-stimulated insulin secretion), and (iv) improvement of beta cells mitochondrial physiological functions. The experiments were carried out using rat beta INS-1E cell line in the presence or absence of bergenin and a cocktail of proinflammatory cytokines (interleukin-1beta, tumor necrosis factor-alpha, and interferon- gamma) for 48 hr. Bergenin significantly inhibited beta cell apoptosis, as inferred from the reduction in the caspase-3 activity (IC50 = 7.29 ± 2.45 μM), and concurrently increased cellular ATP Levels (EC50 = 1.97 ± 0.47 μM). Bergenin also significantly enhanced insulin secretion (EC50 = 6.73 ± 2.15 μM) in INS-1E cells, presumably because of the decreased nitric oxide production (IC50 = 6.82 ± 2.83 μM). Bergenin restored mitochondrial membrane potential (EC50 = 2.27 ± 0.83 μM), decreased ROS production (IC50 = 14.63 ± 3.18 μM), and improved mitochondrial dehydrogenase activity (EC50 = 1.39 ± 0.62 μM). This study shows for the first time that bergenin protected beta cells from cytokine-induced apoptosis and restored insulin secretory function by virtue of its anti-inflammatory, antioxidant and anti-apoptotic properties. To sum up, the above mentioned data highlight bergenin as a promising anti-apoptotic agent in the context of diabetes.

scholarly journals THE ROLE OF SURVIVIN AND RAF-1 KINASE AGAINST ENHANCEMENT OF PANCREATIC BETA-CELL APOPTOSIS IN PATIENTS WITH TYPE 2 DIABETES MELLITUS

2018 ◽  
Vol 11 (11) ◽  
pp. 344
Author(s):  
Eva Decroli ◽  
Asman Manaf ◽  
Syafril Syahbuddin ◽  
Sarwono Waspadji ◽  
Dwisari Dillasamola
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Beta Cell ◽  
Cell Apoptosis ◽  
Pancreatic Beta Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Beta Cell Apoptosis

Objective: This study aimed to reveal differences in levels of survivin and Raf-1 kinase in prediabetes, controlled Type 2 diabetes mellitus (T2DM), uncontrolled T2DM, and their relationship with hemoglobin A1c (HbA1c) levels and serum triglyceride levels.Methods: This study was an observational study with a cross-sectional design. The study involved 60 people with T2DM who visited the endocrine and metabolic clinic and 30 prediabetes patients. The variables were survivin levels and Raf-1 kinase enzymes that examined using enzyme-linked immunosorbent assay techniques. HbA1c values are measured by high-performance liquid chromatography and triglyceride levels measured by enzymatic method.Results: Average levels of Raf-1 kinase were significantly higher in the prediabetes group, controlled T2DM, and uncontrolled T2DM (11.6±1.4 pg mL, 9.9±1.1 pg/mL, and 9.1±1.5 pg/mL). Survivin was significantly higher in the prediabetes group, controlled T2DM, and uncontrolled T2DM (5.4±0.4 pg mL, 5.0±0.2 pg/mL, and 4.7±0.1 pg/mL). There was no correlation between HbA1c with Raf-1 kinase levels (R=−0.215, p=0.250), but there was a correlation between HbA1c with serum survivin levels (R=−0.6, *p<0.05). There was a correlation between the levels of triglycerides with survivin but not with Raf-1 kinase (R=−0.267, *p=0.039).Conclusion: Survivin and Raf-1 kinase levels are lower in uncontrolled T2DM. This explained the role of survivin and Raf-1 kinase against enhancement of pancreatic beta-cell apoptosis in patients with T2DM.

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