scholarly journals Prolonged exposure of human pancreatic islets to high glucose concentrations in vitro impairs the beta-cell function.

1992 ◽  
Vol 90 (4) ◽  
pp. 1263-1268 ◽  
Author(s):  
D L Eizirik ◽  
G S Korbutt ◽  
C Hellerström
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Beta Cell Function ◽  
Prolonged Exposure ◽  
Cell Function ◽  
Human Pancreatic Islets

scholarly journals Preservation of Beta cell function in adult human pancreatic islets for several months in vitro

Diabetologia ◽  
1979 ◽  
Vol 16 (2) ◽  
pp. 97-100 ◽  
Author(s):  
J. H. Nielsen ◽  
J. Brunstedt ◽  
A. Andersson ◽  
C. Frimodt-M�ller
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Beta Cell Function ◽  
Cell Function ◽  
Human Pancreatic Islets ◽  
Adult Human

scholarly journals Pancreatic islets of bank vole show signs of dysfunction after prolonged exposure to high glucose concentrations in vitro

2010 ◽  
Vol 206 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Martin Blixt ◽  
Bo Niklasson ◽  
Stellan Sandler
Keyword(s):  
Gender Difference ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Prolonged Exposure ◽  
Cell Function ◽  
Insulin Biosynthesis ◽  
Bank Voles ◽  
Glucose Tolerant ◽  
Β Cell Function

Bank voles develop glucose intolerance/diabetes mellitus when kept in captivity. We have characterized β-cell function of glucose intolerant/diabetic animals, and found that this animal model has features of both human type 1 and type 2 diabetes. The aim of this study was to study the functional alterations of islets isolated from glucose tolerant bank voles after a prolonged exposure to various glucose concentrations in vitro. For this purpose, pancreatic islets from normal (glucose tolerant) male and female bank voles were cultured at different glucose concentrations (5.6, 11.1 (control), or 28 mM) whereupon islet functions were examined. Overall, islet insulin output was lowered at 5.6 mM glucose, and similar to control, or enhanced after culture in 28 mM glucose. High glucose culture led to decreased insulin contents, but there was no change in islet DNA content and in morphological assessments of cell death, with the latter findings suggesting that the so-called glucotoxicity had not evolved. A slight gender difference was observed in that islets isolated from females exhibited a glucose-regulated (pro)insulin biosynthesis rate and insulin gene expression. In conclusion, we have found that islets isolated from female and male bank voles are affected by glucose concentrations in vitro in that some signs of dysfunction were observed upon high glucose exposure. A minor gender difference was observed suggesting that the islets of the females may more readily adapt to the elevated glucose concentration than islets of the male bank voles. It could be that these in vitro gender differences observed may represent a mechanism underlying the gender difference in diabetes development observed among bank voles.

Glucose transporter 2 gene polymorphisms and beta-cell function in isolated human pancreatic islets

2009 ◽  
Vol 35 (2) ◽  
pp. 155-156 ◽  
Author(s):  
S. Del Guerra ◽  
R. Lupi ◽  
V. D’Aleo ◽  
F. Filipponi ◽  
U. Boggi ◽  
...  
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Beta Cell Function ◽  
Gene Polymorphisms ◽  
Glucose Transporter ◽  
Cell Function ◽  
Human Pancreatic Islets ◽  
Glucose Transporter 2

scholarly journals Class IIa HDACs do not influence beta-cell function under normal or high glucose conditions

Islets ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 112-118
Author(s):  
Jacob McCann ◽  
Megan Ellis ◽  
Sean L. McGee ◽  
Kathryn Aston-Mourney
Keyword(s):  
Beta Cell ◽  
High Glucose ◽  
Beta Cell Function ◽  
Cell Function ◽  
Class Iia Hdacs

Impaired beta-cell functions induced by chronic exposure of cultured human pancreatic islets to high glucose

Diabetes ◽  
1999 ◽  
Vol 48 (6) ◽  
pp. 1230-1236 ◽  
Author(s):  
S. Marshak ◽  
G. Leibowitz ◽  
F. Bertuzzi ◽  
C. Socci ◽  
N. Kaiser ◽  
...  
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Chronic Exposure ◽  
Human Pancreatic Islets ◽  
Cell Functions

scholarly journals Insulin-sparing effects of troglitazone in rat pancreatic islets

2003 ◽  
Vol 31 (1) ◽  
pp. 61-69 ◽  
Author(s):  
LC Bollheimer ◽  
S Troll ◽  
H Landauer ◽  
CE Wrede ◽  
J Scholmerich ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Cell Function ◽  
Glucagon Secretion ◽  
Point Of View ◽  
Glucose Levels ◽  
Rat Pancreatic Islets ◽  
Insulin And Glucagon Secretion

Thiazolidinediones (TZDs) have been suggested to act beneficially on pancreatic islet function and on beta-cell viability but data concerning direct effects on isolated islets are controversial. Therefore, we have examined parameters of pancreatic insulin and glucagon secretion and biosynthesis in TZD-exposed rat pancreatic islets under physiological glucose level conditions and under conditions of glucolipotoxicity. Primary rat islets were incubated for 2.5 h with or without troglitazone (10 microM) in 5.6 mM glucose (standard glucose levels) and 16.7 mM glucose (high glucose levels); a subgroup was additionally treated with oleate (200 microM) to simulate acute glucolipotoxicity. Insulin and glucagon secretion, intracellular content and their respective mRNAs were quantified. Newly synthesized insulin was determined by pulse-labeling experiments. Troglitazone reduced insulin secretion at standard and high glucose levels by about one-third (P<or=0.05). Insulin content was decreased at 5.6 mM glucose but increased at 16.7 mM glucose by the presence of troglitazone (P<or=0.05). Newly synthesized insulin mRNA and preproinsulin mRNA decreased by about 20% at standard glucose levels (P<or=0.05). Glucagon secretion was augmented by troglitazone in islets under high glucose conditions by an additional 50% (P<or=0.05). No clear beneficial troglitazone effects were observed under glucolipotoxic conditions. The reduced insulin secretion and biosynthesis at standard glucose levels can be interpreted as an insulin-sparing effect. Troglitazone effects were less pronounced at high glucose alone or in combination with oleate. From a clinical point of view, these results indicate a greater benefit of troglitazone for beta-cell function in hyperinsulinemic, but normoglycemic patients with insulin resistance or early type 2 diabetes without major insulin secretion deficits and/or pronounced hyperglycemia.

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