Factors Affecting the Uptake of Glibenclamide in Microdissected Pancreatic Islets Rich in β-Cells

Pharmacology ◽  
1974 ◽  
Vol 11 (5) ◽  
pp. 257-267 ◽  
Author(s):  
Bo Hellman
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells ◽  
Factors Affecting ◽  
Microdissected Pancreatic Islets

IONIC EFFECTS ON THE UPTAKE OF CHLOROMERCURIBENZENE-p-SULPHONIC ACID BY PANCREATIC ISLETS

1977 ◽  
Vol 86 (3) ◽  
pp. 552-560 ◽  
Author(s):  
Monica Söderberg ◽  
Inge-Bert Täljedal
Keyword(s):  
Pancreatic Islets ◽  
Islet Cell ◽  
Choline Chloride ◽  
Inorganic Ions ◽  
Sulphonic Acid ◽  
Cell Uptake ◽  
Β Cells ◽  
Sulphydryl Groups ◽  
Microdissected Pancreatic Islets ◽  
Ionic Effects

ABSTRACT Effects of inorganic ions on the uptake of chloromercuribenzene-p-sulphonic acid (CMBS) were studied in microdissected pancreatic islets of non-inbred ob/ob-mice. Na2SO4 stimulated the total islet cell uptake of CMBS but decreased the amount of CMBS remaining in islets after brief washing with L-cysteine. CaCl2 stimulated both the total and the cysteine-non-displaceable uptake; the stimulatory effect of CaCl2 on the cysteine-non-displaceable CMBS uptake was counteracted by Na2SO4. NaCl, KCl or choline chloride had no significant effect on the total islet cell uptake of CMBS, whereas LiCl was stimulatory. It is concluded that β-cells resemble erythrocytes in having a permeation path for CMBS that is inhibited by SO42−. By analogy with existing models of the erythrocyte membrane, it is suggested that the SO42−-sensitive path leads to sulphydryl groups controlling monovalent cationic permeability in β-cells.

Phosphofructokinase isozymes in pancreatic islets and clonal beta-cells (INS-1)

Diabetes ◽  
1995 ◽  
Vol 44 (11) ◽  
pp. 1285-1289 ◽  
Author(s):  
G. C. Yaney ◽  
V. Schultz ◽  
B. A. Cunningham ◽  
G. A. Dunaway ◽  
B. E. Corkey ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells

scholarly journals Vanadyl Sulfate Treatment Stimulates Proliferation and Regeneration of Beta Cells in Pancreatic Islets

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Samira Missaoui ◽  
Khémais Ben Rhouma ◽  
Mohamed-Tahar Yacoubi ◽  
Mohsen Sakly ◽  
Olfa Tebourbi
Keyword(s):  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Control Level ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Dependent Manner ◽  
Glucose Levels ◽  
Blood Glucose Levels

We examined the effects of vanadium sulfate (VOSO4) treatment at 5 and 10 mg/kg for 30 days on endocrine pancreas activity and histology in nondiabetic and STZ-induced diabetic rats. In diabetic group, blood glucose levels significantly increased while insulinemia level markedly decreased. At the end of treatment, VOSO4at a dose of 10 mg/Kg normalized blood glucose level in diabetic group, restored insulinemia, and significantly improved insulin sensitivity. VOSO4also increased in a dose-dependent manner the number of insulin immunopositive beta cells in pancreatic islets of nondiabetic rats. Furthermore, in the STZ-diabetic group, the decrease in the number of insulin immunopositive beta cells was corrected to reach the control level mainly with the higher dose of vanadium. Therefore, VOSO4treatment normalized plasma glucose and insulin levels and improved insulin sensitivity in STZ-experimental diabetes and induced beta cells proliferation and/or regeneration in normal or diabetic rats.

scholarly journals Virgin Beta Cells Persist throughout Life at a Neogenic Niche within Pancreatic Islets

2017 ◽  
Vol 25 (4) ◽  
pp. 911-926.e6 ◽  
Author(s):  
Talitha van der Meulen ◽  
Alex M. Mawla ◽  
Michael R. DiGruccio ◽  
Michael W. Adams ◽  
Vera Nies ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells

Expression, localization and functional role of small GTPases of the Rab3 family in insulin-secreting cells

1996 ◽  
Vol 109 (9) ◽  
pp. 2265-2273 ◽  
Author(s):  
R. Regazzi ◽  
M. Ravazzola ◽  
M. Iezzi ◽  
J. Lang ◽  
A. Zahraoui ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells ◽  
Insulin Release ◽  
Cell Lines ◽  
Secretory Granules ◽  
Small Gtpases ◽  
Wild Type ◽  
Gtp Hydrolysis ◽  
Human Pancreatic Islets ◽  
Insulin Secreting Cells

We examined the presence of small molecular mass GTP-binding proteins of the Rab3 family in different insulin-secreting cells. Rab3B and Rab3C were identified by western blotting in rat and in human pancreatic islets, in two rat insulin-secreting cell lines, RINm5F and INS-1, as well as in the hamster cell line HIT-T15. In contrast, Rab3A was detected in rat pancreatic islets as well as in the two insulin-secreting rat cell lines but not in human pancreatic islets and was only barely discernible in HIT-T15 cells. These findings were confirmed by two-dimensional gel electrophoresis followed by GTP-overlay of homogenates of pancreatic islets and of the purified protein. Northern blotting analysis revealed that Rab3D is expressed in the same insulin-secreting cells as Rab3A. Separation of the cells of the rat islets by fluorescence-activated cell sorting demonstrated that Rab3A was exclusively expressed in beta-cells. Rab3A was found to be associated with insulin-containing secretory granules both by immunofluorescence, immunoelectron microscopy and after sucrose density gradient. Overexpression in HIT-T15 cells of a Rab3A mutant deficient in GTP hydrolysis inhibited insulin secretion stimulated by a mixture of nutrients and bombesin. Insulin release triggered by these secretagogues was also slightly decreased by the overexpression of wild-type Rab3A but not by the overexpression of wild-type Rab5A and of a Rab5A mutant deficient in GTP hydrolysis. Finally, we studied the expression in insulin-secreting cells of rabphilin-3A, a putative effector protein that associates with the GTP-bound form of Rab3A. This Rab3A effector was not detectable in any of the cells investigated in the present study. Taken together these results indicate an involvement of Rab3A in the control of insulin release in rat and hamster. In human beta-cells, a different Rab3 isoform but with homologous function may replace Rab3A.

Polyclonal origin of pancreatic islets in aggregation mouse chimaeras

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1115-1121 ◽  
Author(s):  
L. Deltour ◽  
P. Leduque ◽  
A. Paldi ◽  
M.A. Ripoche ◽  
P. Dubois ◽  
...  
Keyword(s):  
Cell Division ◽  
Pancreatic Islets ◽  
Progenitor Cells ◽  
Beta Cells ◽  
Growth Pattern ◽  
Pancreatic Beta Cells ◽  
Progenitor Cell ◽  
Histological Sections ◽  
Small Clusters

In the present study, we have examined the origin and growth pattern of the beta cells in pancreatic islets, to determine whether a single progenitor cell gave rise to all the precursors of the islets, or if each of a few progenitor cells is the founder of a different islet, or if each islet is a mixture of cells originating from a pool of progenitor cells. Aggregation mouse chimaeras where the pancreatic beta cells derived from each embryo can be identified in the islets on histological sections were analyzed. In two chimaeras, all the islets contained cells from both the aggregated embryo. This clearly demonstrates that each islet resulted from several independent cells. In addition, the beta cells derived from either embryo component were in very small clusters in the islets, suggesting that in situ cell division did not account significantly for islet growth.

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.

In vivoandex vivo19-fluorine magnetic resonance imaging and spectroscopy of beta-cells and pancreatic islets using GLUT-2 specific contrast agents

2016 ◽  
Vol 11 (6) ◽  
pp. 506-513 ◽  
Author(s):  
Sayuan Liang ◽  
Karim Louchami ◽  
Hauke Kolster ◽  
Anna Jacobsen ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Contrast Agents ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Resonance Imaging ◽  
Imaging And Spectroscopy ◽  
Fluorine Magnetic Resonance Imaging

scholarly journals Cx36 preferentially connects beta-cells within pancreatic islets

Diabetes ◽  
2000 ◽  
Vol 49 (5) ◽  
pp. 727-734 ◽  
Author(s):  
V. Serre-Beinier ◽  
S. Le Gurun ◽  
N. Belluardo ◽  
A. Trovato-Salinaro ◽  
A. Charollais ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells
Sign in / Sign up

Export Citation Format

Share Document