scholarly journals Mechanisms of the stimulation of insulin release by arginine-vasopressin in normal mouse islets.

1990 ◽  
Vol 265 (26) ◽  
pp. 15724-15730
Author(s):  
Z.Y. Gao ◽  
G. Drews ◽  
M. Nenquin ◽  
T.D. Plant ◽  
J.C. Henquin
Keyword(s):  
Insulin Release ◽  
Arginine Vasopressin ◽  
Normal Mouse ◽  
Mouse Islets ◽  
Stimulation Of

scholarly journals Vanadate stimulation of insulin release in normal mouse islets.

1991 ◽  
Vol 266 (32) ◽  
pp. 21649-21656
Author(s):  
A.Q. Zhang ◽  
Z.Y. Gao ◽  
P. Gilon ◽  
M. Nenquin ◽  
G. Drews ◽  
...  
Keyword(s):  
Insulin Release ◽  
Normal Mouse ◽  
Mouse Islets ◽  
Stimulation Of

Relative Importance of Extracellular and Intracellular Ca2+ for Acetylcholine Stimulation of Insulin Release in Mouse Islets

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 198-204 ◽  
Author(s):  
M. P. Hermans ◽  
J.-C. Henquin
Keyword(s):  
Insulin Release ◽  
Relative Importance ◽  
Mouse Islets ◽  
Stimulation Of

scholarly journals Multiple effects and stimulation of insulin secretion by the tyrosine kinase inhibitor genistein in normal mouse islets

1995 ◽  
Vol 114 (4) ◽  
pp. 872-880 ◽  
Author(s):  
J.C. Jonas ◽  
T.D. Plant ◽  
P. Gilon ◽  
P. Detimary ◽  
M. Nenquin ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Normal Mouse ◽  
Kinase Inhibitor ◽  
Mouse Islets ◽  
Stimulation Of

scholarly journals Mechanisms of the stimulation of insulin release by oxytocin in normal mouse islets

1991 ◽  
Vol 276 (1) ◽  
pp. 169-174 ◽  
Author(s):  
Z Y Gao ◽  
G Drews ◽  
J C Henquin
Keyword(s):  
B Cells ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Islet Cells ◽  
Inositol Phosphate ◽  
Resting Potential ◽  
Phosphoinositide Metabolism ◽  
Mouse Islets ◽  
45Ca Efflux ◽  
Stimulation Of

Oxytocin (OT) produced a dose-dependent increase in somatostatin, glucagon and insulin release by isolated mouse islets. A small effect on somatostatin release was observed with 0.1 nM-OT, but 1-10 nM-OT was required to affect A- and B- cells significantly. The effects of OT on somatostatin and glucagon release were similar in the presence of 3 mM- and 10 mM-glucose. No change in insulin release was produced by OT in 3 mM-glucose, but a stimulation was still observed in the presence of a maximally effective concentration of glucose (30 mM). The increase in insulin release produced by OT (in 15 mM-glucose) was accompanied by small accelerations of 86Rb and 45Ca efflux from islet cells. Omission of extracellular Ca2+ accentuated the effect of OT on 86Rb efflux, attenuated that on 45Ca efflux, and abolished that on release. OT never inhibited 86Rb efflux. It did not affect the resting potential of B-cells, but slightly increased the Ca2(+)-dependent electrical activity induced by 15 mM-glucose. OT did not affect cyclic AMP levels, but increased inositol phosphate levels in islet cells. It is suggested that the amplification of glucose-induced insulin release that OT produces is due to a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than to a change in cyclic AMP levels or a direct action on the membrane potential. Since OT is present in the pancreas, it is possible that it exerts a neuropeptidergic control of the islet function.

scholarly journals Effect of interferon and double-stranded RNA on B-cell function in mouse islets of Langerhans

1985 ◽  
Vol 228 (1) ◽  
pp. 87-94 ◽  
Author(s):  
C J Rhodes ◽  
K W Taylor
Keyword(s):  
Insulin Release ◽  
Cell Function ◽  
Protein Biosynthesis ◽  
Insulin Biosynthesis ◽  
Double Stranded Rna ◽  
Mouse Pancreatic Islets ◽  
Mouse Islets ◽  
Stimulation Of ◽  
Slight Inhibition

The direct effects of alpha- and beta-interferons on isolated mouse pancreatic islets were investigated in vitro and found to be similar. After 7 h incubation with interferon concentrations above 350 units/ml, glucose-stimulated (pro)insulin biosynthesis was significantly inhibited, with only a slight inhibition of total protein biosynthesis. Inhibition could be abolished in the additional presence of an anti-interferon antibody. Interferon did not affect insulin release, total insulin content, or glucose oxidation of the islets. The stimulation of (pro)insulin biosynthesis by adenosine, D-glyceraldehyde, mannose, N-acetylglucosamine and leucine was also inhibited by interferon, with no effect on insulin release. At concentrations of dsRNA (double-stranded RNA) said to induce interferon (1-100 micrograms/ml), glucose-stimulated (pro)insulin biosynthesis was inhibited without significantly affecting insulin release. The dsRNA may itself inhibit stimulated (pro)insulin biosynthesis or may function indirectly by the induction of interferon.

scholarly journals Insulin release from mouse islets. Effect of glucose and hormones on adenylate cyclase

1972 ◽  
Vol 129 (2) ◽  
pp. 373-379 ◽  
Author(s):  
Brian Davis ◽  
Norman R. Lazarus
Keyword(s):  
Adenylate Cyclase ◽  
Insulin Release ◽  
Normal Mouse ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Adenylate Cyclase System ◽  
Ph Optimum ◽  
Mouse Islets ◽  
Triton X ◽  
Effect Of Glucose

The adenylate cyclase system of normal mouse islets was characterized. The pH optimum of the system was 7.6. The enzyme preparation contained particulate phosphodiesterase activity. This could be removed by treatment with 0.4% (v/v) Triton X-100 or inhibited by 8mm-theophylline in the presence of 2mm-cyclic AMP (adenosine 3′:5′-cyclic monophosphate). ATP at 0.32mm produced one-half maximal enzyme activity. The enzyme was stimulated in the presence of F-and strongly inhibited by Ca2+. The isolated enzyme retained hormonal sensitivity and was stimulated by glucagon, pancreozymin and secretin at physiological concentrations. Glucose at 17mm, 8mm and 2mm had no direct effect on the activity of the enzyme; neither did galactose at the same concentrations. Groups of islets incubated in 17mm- or 2mm-glucose for 5 or 15min and then homogenized and assayed for adenylate cyclase activity showed no differences in adenylate cyclase activity. The results suggest that the mechanism of glucose-mediated insulin release is not via the adenylate cyclase system. Hormones, however, could mediate insulin secretion via their effects on the adenylate cyclase system.

Arginine Vasopressin and Oxytocin Effects in Mouse Pancreatic  -cells: Receptors Involved in Stimulation of Insulin Release

Diabetes ◽  
1993 ◽  
Vol 42 (6) ◽  
pp. 914-921 ◽  
Author(s):  
Z.-Y. Gao ◽  
J.-C. Henquin
Keyword(s):  
Insulin Release ◽  
Arginine Vasopressin ◽  
Pancreatic Cells ◽  
Stimulation Of

Relative importance of extracellular and intracellular Ca2+ for acetylcholine stimulation of insulin release in mouse islets

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 198-204 ◽  
Author(s):  
M. P. Hermans ◽  
J. C. Henquin
Keyword(s):  
Insulin Release ◽  
Relative Importance ◽  
Mouse Islets ◽  
Stimulation Of

scholarly journals Glucose-, calcium- and concentration-dependence of acetylcholine stimulation of insulin release and ionic fluxes in mouse islets

1988 ◽  
Vol 254 (1) ◽  
pp. 211-218 ◽  
Author(s):  
M C Garcia ◽  
M P Hermans ◽  
J C Henquin
Keyword(s):  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Physiological Conditions ◽  
Ionic Fluxes ◽  
Low Glucose ◽  
Mouse Islets ◽  
High Concentrations ◽  
Glucose Dependence ◽  
Stimulation Of

Mouse islets were used to define the glucose-dependence and extracellular Ca2+ requirement of muscarinic stimulation of pancreatic beta-cells. In the presence of a stimulatory concentration of glucose (10 mM) and of Ca2+, acetylcholine (0.1-100 microM) accelerated 3H efflux from islets preloaded with myo-[3H]inositol. It also stimulated 45Ca2+ influx and efflux, 86Rb+ efflux and insulin release. In the absence of Ca2+, only 10-100 microM-acetylcholine mobilized enough intracellular Ca2+ to trigger an early but brief peak of insulin release. At a non-stimulatory concentration of glucose (3 mM), 1 microM- and 100 microM-acetylcholine increased 45Ca2+ and 86Rb+ efflux in the presence and absence of extracellular Ca2+. However, only 100 microM-acetylcholine marginally increased 45Ca2+ influx and caused a small, delayed, stimulation of insulin release, which was abolished by omission of Ca2+. At a maximally effective concentration of glucose (30 mM), 1 microM- and 100 microM-acetylcholine increased 45Ca2+ influx and efflux only slightly, but markedly amplified insulin release. Again, only 100 microM-acetylcholine mobilized enough Ca2+ to trigger a peak of insulin release in the absence of Ca2+. The results thus show that only high concentrations of acetylcholine (greater than or equal to 10 microM) can induce release at low glucose or in a Ca2+-free medium. beta-Cells exhibit their highest sensitivity to acetylcholine in the presence of Ca2+ and stimulatory glucose. Under these physiological conditions, the large amplification of insulin release appears to be the result of combined effects of the neurotransmitter on Ca2+ influx, on intracellular Ca2+ stores and on the efficiency with which Ca2+ activates the releasing machinery.

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