scholarly journals Effects of L-leucine on the insulin production, oxidative metabolism and mitochondrial ultrastructure of isolated mouse pancreatic islets in tissue culture

Diabetologia ◽  
1977 ◽  
Vol 13 (1) ◽  
pp. 59-69 ◽  
Author(s):  
A. Andersson ◽  
J. H�iriis-Nielsen ◽  
L. A. H. Borg
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Oxidative Metabolism ◽  
Insulin Production ◽  
Mitochondrial Ultrastructure ◽  
Mouse Pancreatic Islets

scholarly journals Long-term effects of glucose on insulin release and glucose oxidation by mouse pancreatic islets maintained in tissue culture

1974 ◽  
Vol 140 (3) ◽  
pp. 377-382 ◽  
Author(s):  
Arne Andersson
Keyword(s):  
Tissue Culture ◽  
B Cells ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
High Glucose ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Mouse Pancreatic Islets

Rates of glucose oxidation and insulin release in response to a wide range of glucose concentrations were studied in short-term experiments in isolated mouse pancreatic islets maintained in tissue culture for 6 days at either a physiological glucose concentration (6.7mm) or at a high glucose concentration (28mm). The curves relating glucose oxidation or insulin release to the extracellular glucose concentration obtained with islets cultured in 6.7mm-glucose displayed a sigmoid shape similar to that observed for freshly isolated non-cultured islets. By contrast islets that had been cultured in 28mm-glucose showed a linear relationship between the rate of glucose oxidation and the extracellular glucose concentration up to about 8mm-glucose. The maximal oxidative rate was twice that of the non-cultured islets and the glucose concentration associated with the half-maximal rate considerably decreased. In islets cultured at 28mm-glucose there was only a small increase in the insulin release in response to glucose, probably due to a depletion of stored insulin in those B cells that had been cultured in a high-glucose medium. It is concluded that exposure of B cells for 6 days to a glucose concentration comparable with that found in diabetic individuals causes adaptive metabolic alterations rather than degeneration of these cells.

scholarly journals Opposite effects of starvation on oxidation of [14C]adenosine and adenosine-induced insulin release by isolated mouse pancreatic islets

1978 ◽  
Vol 176 (2) ◽  
pp. 619-621 ◽  
Author(s):  
A Andersson
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Metabolic Flux ◽  
Insulin Biosynthesis ◽  
Insulin Production ◽  
Stimulate Insulin Secretion ◽  
Mouse Pancreatic Islets

To test further the hypothesis that ribonucleosides stimulate insulin secretion and biosynthesis by producing metabolic signals, the effects of starvation on adenosine-stimulated insulin production and the oxidation of adenosine by isolated mouse pancreatic islets were examined. No direct correlation was found between the metabolic flux and insulin secretion, since the starvation-induced impairment of the adenosine-stimulated insulin secretion was accompanied by an increased rate of adenosine oxidation. Adenosine-stimulated insulin biosynthesis was, however, unaffected by starvation.

Effects of starvation on oxidative metabolism and insulin release by isolated mouse pancreatic islets

1982 ◽  
Vol 101 (2) ◽  
pp. 227-234 ◽  
Author(s):  
Michael Welsh ◽  
Arne Andersson
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Oxidative Metabolism ◽  
Oxidation Rate ◽  
Insulin Response ◽  
Leucine Oxidation ◽  
Oxidation Rates ◽  
Impaired Insulin ◽  
Mouse Pancreatic Islets ◽  
Insulin Response To Glucose

Abstract. Pancreatic islets were isolated from either 60-h-starved or fed mice and subsequently incubated in order to determine the insulin release in response to various secretagogues, rates of glucose, leucine or glutamine oxidation or the acetoacetate production from leucine. It was found that in contrast to findings with islets isolated from fed mice 16.7 mm glucose, 10 mM leucine and 10 mm α-ketoisocaproic acid did not stimulate the insulin release of islets isolated from starved mice. Moreover, the insulin release in response to leucine plus glutamine or glucose plus glutamine was decreased after starvation although these values were higher than those obtained for glutamine addition alone. Theophylline, however, restored partly the impaired insulin response to glucose and completely that to leucine or α-ketoisocaproic acid. Starvation was found to inhibit the islet glucose oxidation rate but the addition of theophylline was without effect irrespective of whether the islets were prepared from fed or starved mice. On the contrary, islet leucine oxidation was increased after starvation and again theophylline did not affect the islet leucine oxidation rate. Likewise, the islet acetoacetate production was increased after starvation. The glutamine oxidation rates were not affected by starvation, either when tested alone or together with glucose or leucine. It is concluded that although the starvation-induced impairment of glucose-stimulated insulin release may well be explained by an influence on the oxidative metabolism other factors are also involved as regards leucine-stimulated insulin release.

Direct long-term effect of hydrocortisone on insulin and glucagon release from mouse pancreatic islets in tissue culture

1981 ◽  
Vol 96 (4) ◽  
pp. 498-504 ◽  
Author(s):  
J. Brunstedt ◽  
J. Høiriis Nielsen
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Endocrine Function ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Long Term Effect ◽  
Mouse Pancreatic Islets ◽  
Pancreatic Endocrine Function ◽  
Mouse Islets

Abstract. The effects of glucocorticoids on the pancreatic endocrine function was studied in isolated mouse pancreatic islets maintained in tissue culture for 1 to 3 weeks. Following culture for 1 week without corticoid supplement acute experiments with hydrocortisone showed no significant effect on the glucose-induced insulin release at 10−8 to 10−5 mol/l hydrocortisone. When, however, the islets were cultured in the presence of hvdrocortisone, there was an increased insulin release to the medium in a dose-dependent manner, with the maximal effect at 10−7 mol/l hydrocortisone. The release of glucagon to the medium was not affected to the same degree, but showed a slight inhibition at increasing concentrations of hydrocortisone. Short-term experiments after the culture period showed that islets cultured for 3 weeks in the presence of 10−7 to 10−5 mol/l hydrocortisone had an enhanced insulin secretion in response to glucose. The islets did not show any statistically significant change in their insulin- and DNA-content after 3 weeks of culture with hydrocortisone, but a marked reduction in the content of glucagon was found with increasing concentrations of hydrocortisone. The present results suggest that physiological concentrations of hydrocortisone are of importance for mouse islets to maintain their insulin production in tissue culture.

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