scholarly journals Effect of Human Islet Rescue Gradient Purification on Islet Yield and Fractional Beta Cell Viability

2008 ◽  
Vol 40 (2) ◽  
pp. 360-361 ◽  
Author(s):  
A. Miki ◽  
C. Ricordi ◽  
T. Yamamoto ◽  
A. Mita ◽  
S. Barker ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Viability ◽  
Human Islet ◽  
Beta Cell Viability

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

scholarly journals A Novel Method for the Assessment of Cellular Composition and Beta-Cell Viability in Human Islet Preparations

2005 ◽  
Vol 5 (7) ◽  
pp. 1635-1645 ◽  
Author(s):  
Hirohito Ichii ◽  
Luca Inverardi ◽  
Antonello Pileggi ◽  
R. Damaris Molano ◽  
Over Cabrera ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Viability ◽  
Human Islet ◽  
Cellular Composition ◽  
Novel Method ◽  
Beta Cell Viability

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 The transcription factor STAT6 plays a critical role in promoting beta cell viability and is depleted in islets of individuals with type 1 diabetes

Diabetologia ◽  
2018 ◽  
Vol 62 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Kaiyven A. Leslie ◽  
Mark A. Russell ◽  
Kazuto Taniguchi ◽  
Sarah J. Richardson ◽  
Noel G. Morgan
Keyword(s):  
Type 1 Diabetes ◽  
Transcription Factor ◽  
Beta Cell ◽  
Cell Viability ◽  
Critical Role ◽  
Beta Cell Viability

scholarly journals The role of coffee derivatives in the regulation of pancreatic beta cell function in Type 2 Diabetes

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Kittiwadee Sarnsamak ◽  
Adele Costabile ◽  
Astrid Hauge-Evans
Keyword(s):  
Type 2 Diabetes ◽  
Beta Cell ◽  
Cell Viability ◽  
Ferulic Acid ◽  
Beta Cells ◽  
Secretory Function ◽  
Atp Content ◽  
Beta Cell Viability

AbstractCoffee contains several components other than caffeine such as chlorogenic acids (CGAs), which are a family of polyphenols. Non-caffeinated coffee has been shown to reduce the risk of Type 2 diabetes, but it is unclear whether this effect is primarily due to a beneficial action on glucose regulation in peripheral tissues or whether it is partly mediated via a direct, functional modulation of insulin-secreting beta cells from the pancreas. This study aims to explore the specific role of coffee compounds derived from the polyphenolic family of CGAs (caffeic acid (CA) and ferulic acid (FA)) and their metabolites (dihydroferulic acid (diFA) and ferulic acid 4-O-sulphate (FA-4-OS)) in the regulation of beta cell survival and secretory function. To investigate this role, the cells were initially exposed to conditions of glucotoxicity (30mmol/l glucose), lipotoxicity (0.5mmol/l palmitate), glucolipotoxicity (30mmol/l glucose + 0.5mmol/l palmitate) and cytokine-induced cell toxicity (25U/ml IL1b + 500U/ml TNFα) for 20 and 48 h. INS1 beta cells were subsequently treated with or without 100nmol/l of the CGA compounds for 48 h followed by 20 h exposure to glucolipotoxicity to measure cellular ATP content and 3/7 caspase activity, respectively, as an indication of cell viability and apoptosis. Additionally, insulin release was assessed by radioimmunoassay following 1 h static incubations with or without CA, FA and metabolites. Data were analysed by One-Way ANOVA using GraphPad prism software (version 8). Glucotoxicity, lipotoxicity and glucotoxicity or glucolipotoxicity combined with cytokines significantly reduced INS1 cell viability compared to control at 20 and 48 h (p < 0.001 vs 11mmol/l glucose, p < 0.05; Glucotoxicity vs 11mmol/l glucose at 20 h, n = 6), whereas cytokines alone did not significantly affect cellular ATP content. Moreover, pre-treatment for 48 h with CGAs alone or in combination did not affect INS1 beta-cell viability under basal conditions (n = 3, p > 0.2). Additional exposure to glucolipotoxicity for 20 h significantly decreased beta cell viability and survival and was not alleviated by pre- or co-treatment with CGAs (n = 3, p > 0.05). However, insulin release in response to 1 h incubation with 20 mmol/l glucose + 10μmol/l forskolin (FSK) + 100μmol/l 3-isobutyl-1-methylxanthine (IBMX) was significantly higher from cells pre-treated with CA and FA combined compared to controls (7.64 + 2.89pg insulin/5,000 cells/h vs 2.17 + 0.35pg insulin/5,000 cells/h; p < 0.01 vs. 20mmol/l glucose + 10μmol/l FSK + 100μmol/l IBMX only, n = 5). The results suggest that CGA derivatives from coffee do not directly modulate INS1 beta cell viability and apoptosis whereas the compounds may play a role in the regulation of beta cell secretory function.

Assessment of Beta Cell Viability

2011 ◽  
Vol 55 (1) ◽  
Author(s):  
Sundararajan Jayaraman
Keyword(s):  
Beta Cell ◽  
Cell Viability ◽  
Beta Cell Viability

scholarly journals Pharmacological inhibition of thioredoxin reductase increases insulin secretion and diminishes beta cell viability

2021 ◽  
Author(s):  
Dennis Brüning ◽  
Kathrin Hatlapatka ◽  
Verena Lier-Glaubitz ◽  
Vincent Andermark ◽  
Stephan Scherneck ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Viability ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Thioredoxin Reductase ◽  
Dual Function ◽  
Min6 Cells ◽  
Thioredoxin System ◽  
Beta Cell Viability

AbstractApparently, both a decrease in beta cell function and in beta cell mass contribute to the progressive worsening of type 2 diabetes. So, it is of particular interest to define factors which are relevant for the regulation of insulin secretion and at the same time for the maintenance of beta cell mass. The NADPH-thioredoxin system has a candidate role for such a dual function. Here, we have characterized the effects of a highly specific inhibitor of thioredoxin reductase, AM12, on the viability and function of insulin-secreting MIN6 cells and isolated NMRI mouse islets. Viability was checked by MTT testing and the fluorescent live-dead assay. Apoptosis was assessed by annexin V assay. Insulin secretion of perifused islets was measured by ELISA. The cytosolic Ca2+ concentration was measured by the Fura technique. Acute exposure of perifused pancreatic islets to 5 μM AM12 was without significant effect on insulin secretion. Islets cultured for 24 h in 0.5 or 5 μM AM12 showed unchanged basal secretion during perifusion, but the response to 30 mM glucose was significantly enhanced by 5 μM. Twenty-four-hour exposure to 5 μM AM12 proved to be without effect on the viability of MIN6 cells, whereas longer exposure was clearly toxic. Islets were more susceptible, showing initial signs of apoptosis after 24-h exposure to 5 μM AM12. The activity of the NADPH-thioredoxin system is indispensable for beta cell viability but may have a limiting effect on glucose-induced insulin secretion.

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