scholarly journals Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress

2013 ◽  
Vol 58 (3) ◽  
pp. 447-456 ◽  
Author(s):  
María Ángeles Martín ◽  
Elisa Fernández-Millán ◽  
Sonia Ramos ◽  
Laura Bravo ◽  
Luis Goya
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Cell Viability ◽  
Pancreatic Beta Cell ◽  
And Function ◽  
Beta Cell Viability

scholarly journals Enhancement of homocysteine toxicity to insulin-secreting BRIN-BD11 cells in combination with alloxan

2012 ◽  
Vol 214 (2) ◽  
pp. 233-238 ◽  
Author(s):  
S M J Scullion ◽  
E Gurgul-Convey ◽  
M Elsner ◽  
S Lenzen ◽  
P R Flatt ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Viability ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Control Culture ◽  
Insulin Secreting Cells ◽  
Diphenyl Tetrazolium Bromide ◽  
And Function

Previous studies have shown that homocysteine (HC) has a detrimental impact on insulin secretion and pancreatic beta cell function. The aim of the present study was to determine the role of reactive oxygen species (ROS) in the in vitro toxic effects of HC on insulin secretion and function of BRIN-BD11 insulin-secreting cells. In this study, insulin secretion from BRIN-BD11 cells was determined radioimmunologically, cell viability by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and glucokinase activity by a glucose phosphorylation assay following culture with HC plus alloxan (Alx). Treatment with HC resulted in concentration-dependent inhibition of insulin secretion induced by glucose and other insulinotropic agents. HC in combination with Alx resulted in a more pronounced decline in insulin secretion, including that induced by 20 mM alanine, by 43% (P<0.001) and 30 mM KCl by 60% (P<0.001), compared with control culture. The glucokinase phosphorylating capacity in cells cultured with HC plus Alx was significantly lower, compared with control cells. The cells also displayed a significant 84% (P<0.001) decline in cell viability. Prolonged, 72-h culture of insulin-secreting cells with HC followed by 18-h culture without HC did not result in full restoration of beta cell responses to insulinotropic agents. In vitro oxygen consumption was enhanced by a combination of Alx with HC. The study arrived at the conclusion that HC generates ROS in a redox-cycling reaction with Alx that explains the decline in viability of insulin-secreting cells, leading to reduced glucokinase phosphorylating ability, diminished insulin secretory responsiveness and cell death.

scholarly journals Regulated expression and function of the GABAB receptor in human pancreatic beta cell line and islets

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Latif Rachdi ◽  
Alicia Maugein ◽  
Severine Pechberty ◽  
Mathieu Armanet ◽  
Juliette Hamroune ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Line ◽  
Gabab Receptor ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Regulated Expression ◽  
And Function

W46 ROLE OF LIPOPROTEINS IN PANCREATIC BETA-CELL SURVIVAL, PROLIFERATION AND FUNCTION

2010 ◽  
Vol 11 (2) ◽  
pp. 10
Author(s):  
R.A. Sibler ◽  
S. Rütti ◽  
J.A. Ehses ◽  
R. Prazak ◽  
D.T. Meier ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Pancreatic Beta Cell ◽  
And Function

Prenatal androgen excess impairs beta cell function by decreased Sirtuin3 expression

2021 ◽  
Author(s):  
Yu Zhou ◽  
Min Gong ◽  
Yingfei Lu ◽  
Jianquan Chen ◽  
Rong Ju
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Female Offspring ◽  
Sirtuin 3 ◽  
Prenatal Testosterone ◽  
Pancreatic Beta Cell Function ◽  
Prenatal Androgen

Prenatal androgen exposure induces metabolic disorders in female offspring. However, the long-term effect of maternal testosterone excess on glucose metabolism, especially on pancreatic beta cell function, is rarely investigated. Our current study mainly focused on the effects of prenatal testosterone exposure on glucose metabolism and pancreatic beta cell function in aged female offspring. By using maternal mice and their female offspring as animal models, we found that prenatal androgen treatment induced obesity and glucose intolerance in aged offspring. These influences were accompanied by decreased fasting serum insulin concentration, elevated serum triglyceride and testosterone concentrations. Glucose stimulated insulin secretion in pancreatic beta cells of aged female offspring was also affected by prenatal testosterone exposure. We further confirmed that increased serum testosterone contributed to down regulation of Sirtuin 3 expression, activated oxidative stress and impaired pancreatic beta cell function in aged female offspring. Moreover, over-expression of Sirtuin 3 in islets isolated from female offspring treated with prenatal testosterone normalized the oxidative stress level, restored cyclic adenosine monophosphate and adenosine triphosphate generation, which finally improved glucose stimulated insulin secretion in beta cells. Taken together, these results demonstrated that prenatal testosterone exposure caused metabolic disturbance in aged female offspring via suppression of Sirtuin 3 expression and activation of oxidative stress in pancreatic beta cells.

BENEFICIAL EFFECT OF HUMAN ISLET RESCUE GRADIENT PURIFICATION ON EMBEDDED ISLET AND FRACTIONAL BETA CELL VIABILITY

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 571
Author(s):  
A Miki ◽  
C Ricordi ◽  
T Yamamoto ◽  
A Mita ◽  
S Barker ◽  
...  
Keyword(s):  
Beta Cell ◽  
Beneficial Effect ◽  
Cell Viability ◽  
Human Islet ◽  
Beta Cell Viability
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