Hormone content of mouse pancreatic islets subjected to different in vivo and in vitro functional demands

1981 ◽  
Vol 37 (11) ◽  
pp. 1213-1214 ◽  
Author(s):  
S. Pääbo ◽  
G. Lundqvist ◽  
B. Petersson ◽  
A. Andersson
Keyword(s):  
Pancreatic Islets ◽  
Hormone Content ◽  
Mouse Pancreatic Islets

TRANSPLANTATION OF MOUSE PANCREATIC ISLETS INTO PRIMATES???IN VIVO AND IN VITRO EVALUATION1,2

2001 ◽  
Vol 72 (12) ◽  
pp. 1867-1874 ◽  
Author(s):  
Lionel Badet ◽  
Thomas T. Titus ◽  
Philip McShane ◽  
Li-Way Chang ◽  
Zhenshun Song ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Mouse Pancreatic Islets

Effects of cyclosporin A and verapamil on mouse pancreatic islets

1993 ◽  
Vol 129 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Chun L Shi ◽  
Pål Rooth ◽  
Inge-Bert Täljedal
Keyword(s):  
Cyclosporin A ◽  
Pancreatic Islets ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Nmri Mice ◽  
Mouse Pancreatic Islets ◽  
Beneficial Action ◽  
Primary Interaction

Treatment of NMRI mice with cyclosporin A (25 mg/kg body wt) for 11 days caused a marked fall in pancreas insulin content, although plasma glucose and plasma insulin were unchanged. When islets from untreated mice were exposed to cyclosporin A (2 mg/l) in vitro, no effect was seen in the first hour. After 24 h, cyclosporin A had significantly decreased the islet content of insulin. Post-culture microperifusion showed that cyclosporin A for 24 or 72 h inhibited the insulin secretory responsiveness. Verapamil in vivo (0.4 mg/kg body wt per day) or in vitro (37.5 μg/l) did not modify these effects. Verapamil at 25 mg/l suppressed the release of insulin but afforded no obvious protection against cyclosporin A during culture. The beneficial action of verapamil on islets transplanted to the kidney may reflect renal events rather than a primary interaction of drugs in the islets.

Rapid depletion of somatostatin in isolated mouse pancreatic islets after treatment with cysteamine

1985 ◽  
Vol 110 (2) ◽  
pp. 227-231 ◽  
Author(s):  
Birger Petersson ◽  
Claes Hellerström
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Basal Insulin ◽  
Glucose Stimulation ◽  
Isolated Pancreatic Islets ◽  
Basal Release ◽  
Mouse Pancreatic Islets ◽  
Mouse Islets

Abstract. Cysteamine (CSH; β-mercaptoethylamine) is known to deplete pancreatic somatostatin without affecting the insulin or glucagon content. It may therefore be useful for studies of intra-islet regulation of hormone release. In the present study injection of CSH (60 mg/kg body weight) to mice decreased the somatostatin content of their isolated pancreatic islets to 50% in 1 h and 30% in 4 h as compared to islets of non-injected controls. Exposure of isolated mouse islets to CSH (100 μg/ml) for either 0.5 h followed by incubation in control medium for 3.5 h, or continuously for 4 h, decreased the somatostatin content to about 40% of the controls. There was no change in the islet content of insulin or glucagon. Islets pretreated with CSH (100 μg/ml) for 1 h in vitro showed a decreased glucose stimulation of both oxygen consumption and glucose oxidation. Measurements of insulin release after a similar preincubation of the islets indicated an increased basal release and an attenuated glucose stimulation. It is concluded that CSH rapidly decreases islet somatostatin both in vivo and in vitro. This depletion may lead to a loss of tonic inhibition by islet somatostatin on basal insulin release. It is, however, more plausible that the increased basal insulin release reflected a direct effect of CSH on the islet β-cells.

Persistent impairment of the insulin response to glucose both in vivo and in vitro after streptozotocin exposure: Studies with grafted pancreatic islets and islets maintained in culture

1989 ◽  
Vol 121 (6) ◽  
pp. 849-856 ◽  
Author(s):  
Décio L. Eizirik ◽  
Stellan Sandler ◽  
Olle Korsgren ◽  
Leif Jansson ◽  
Arne Andersson
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Common Property ◽  
Insulin Response ◽  
Insulin Content ◽  
Functional Responses ◽  
Mouse Pancreatic Islets ◽  
Insulin Response To Glucose

Abstract. The functional responses of the pancreatic B-cells after cytotoxic damage are still largely unknown. Using in vitro models to clarify this issue, we have recently observed a preferential reduction of glucose-stimulated insulin production and release in mouse pancreatic islets maintained in culture after in vitro exposure to streptozotocin. In order to evaluate the relevance of these findings in vivo, two sets of experiments were performed. First, mouse pancreatic islets were exposed in vitro to 2.2 mmol/l streptozotocin or vehicle alone, cultured for 6 days, and finally grafted under the kidney capsule of normoglycemic nude mice. Two weeks after transplantation there was no difference in the total DNA and insulin content between the two groups of islet grafts, but the insulin concentration, as expressed per μg DNA, was decreased by 40% in the streptozotocin-treated islets. The insulin release of the grafts, during perfusion of the graft-bearing kidney in situ with 16.7 mmol/l glucose was diminished in the streptozotocin group, whilst perfusion with 16.7 mmol/l glucose plus 5 mmol/l theophylline was able partially to counteract the reduction in insulin release. In the second set of experiments, NMRI mice were injected iv with 160 mg/kg streptozotocin or vehicle alone, and their islets isolated 15 min after the injections. After 6 days in culture, there was no decrease in DNA, glucagon and somatostatin contents, but the insulin content was decreased by 40% in the streptozotocin exposed islets. These islets also showed a 60% decrease in the insulin response to glucose, which was partly counteracted by incubation with 16.7 mmol/1 glucose plus 5 mmol/l theophylline. These observations suggest that a defective response to glucose, in conjunction with a better response to non-nutrient secretagogues, may be a common property of pancreatic islets following toxin-induced disturbances.

Islet Cell Transplantation: In Vivo and in Vitro Functional Assessment of Nonhuman Primate Pancreatic Islets

2000 ◽  
Vol 9 (3) ◽  
pp. 409-414 ◽  
Author(s):  
Alessandra Rammcoli ◽  
Nicola Cautero ◽  
Camillo Ricordi ◽  
Michele Masetti ◽  
Ruth D. Molano ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Cell Transplantation ◽  
Functional Assessment ◽  
Nonhuman Primate ◽  
Islet Cell ◽  
Islet Cell Transplantation

scholarly journals In Vivo Fluorescence Imaging of Blood Flow in Mouse Pancreatic Islets

2011 ◽  
Vol 100 (3) ◽  
pp. 619a
Author(s):  
Kurt W. Short ◽  
W. Steve Head ◽  
Michael McCaughey ◽  
David W. Piston
Keyword(s):  
Blood Flow ◽  
Pancreatic Islets ◽  
Fluorescence Imaging ◽  
In Vivo Fluorescence ◽  
Mouse Pancreatic Islets ◽  
In Vivo Fluorescence Imaging

Mice pancreatic islets protection from oxidative stress induced by single-walled carbon nanotubes through naringin

2018 ◽  
Vol 37 (12) ◽  
pp. 1268-1281 ◽  
Author(s):  
A Ahangarpour ◽  
S Alboghobeish ◽  
AA Oroojan ◽  
MA Dehghani
Keyword(s):  
Oxidative Stress ◽  
Carbon Nanotubes ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Mtt Assay ◽  
Antioxidant Defense System ◽  
Protective Effects ◽  
Cell Functions

The growing use of carbon nanotubes (CNTs) emphasizes the importance of its potential toxic effects on the human health. Previous studies proved that CNTs caused oxidative stress and decreased cell viability. On the other hand, reactive oxygen species (ROS) and oxidative stress impaired β-cell functions and reduced the insulin secretion. However, there is not any study on the effects of CNTs on islets and β-cells. Therefore, the present study aimed to evaluate the effects of single-walled CNTs (SWCNTs) on oxidative stress in islets in addition to the protective effects of naringin (NRG) as an antioxidant . We examined the effects of SWCNTs and naringin on islets by 3,4 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay; measurement of insulin secretion, ROS, and malondialdehyde (MDA); activities of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) peroxidase (GSH-Px); and content of GSH and mitochondrial membrane potential (MMP). The MTT assay demonstrated that decreased viability of islets cells was dose-dependent with exposure to SWCNTs. Further studies revealed that SWCNTs decreased insulin secretion and MMP, induced the formation of ROS, increased the level of MDA, and decreased the activities of SOD, GSH-Px, and CAT and content of GSH. Furthermore, the pretreatment of islets with naringin significantly reverted back these changes. These findings revealed that SWCNTs might induce the oxidative stress to pancreatic islets, causing the occurrence of diabetes, and the protective effects of naringin that was mediated by augmentation of the antioxidant defense system of islets. Our research indicated the necessity for further in vivo and in vitro researches on the effects of SWCNTs and naringin on diabetes.

Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro

1997 ◽  
Vol 155 (2) ◽  
pp. 283-293 ◽  
Author(s):  
A Jorns ◽  
R Munday ◽  
M Tiedge ◽  
S Lenzen
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Ultrastructural Changes ◽  
Cell Necrosis ◽  
High Concentrations ◽  
Beta Cell Necrosis

The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low concentration, destroying all islet cell types at high concentrations. The ultrastructural changes induced by all the test compounds in pancreatic beta cells in vitro were very similar to those observed during the development of alloxan diabetes in vivo. The relative toxicity of the various compounds to pancreatic beta cells in vitro was not, however, related to their ability to cause diabetes in vivo. Indeed, the non-diabetogenic substances ninhydrin, N-butylalloxan and N-isobutylalloxan were very much more toxic to isolated islets than the diabetogenic compounds alloxan and N-methylalloxan. These results suggest that the differences in diabetogenicity among alloxan derivatives are not due to intrinsic differences in the susceptibility of the pancreatic beta cells to their toxicity, but may reflect differences in distribution or metabolism. High concentrations of glucose protected islets against the harmful effects of alloxan and its derivatives, but not those of ninhydrin. Low levels of glucose, and non-carbohydrate nutrients, afforded little protection, indicating that the effect of glucose is not due to the production of reducing equivalents within the cell, 3-O-Methylglucose, which protects against alloan diabetes in vivo, did not protect against alloxan toxicity in vitro. Since 3-O-methylglucose is known to prevent uptake of alloxan by pancreatic beta cells, it appears that uptake of alloxan by the cell is not a prerequisite for the induction of beta cell necrosis.

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