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 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

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 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 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.

STIMULATION OF INSULIN RELEASE BY MAITOTOXIN, AN ACTIVATOR OF VOLTAGE-DEPENDENT CALCIUM CHANNELS

1986 ◽  
Vol 7 (2) ◽  
pp. 107-112 ◽  
Author(s):  
ICHIRO NIKI ◽  
TATSUO TAMAGAWA ◽  
HATSUMI NIKI ◽  
ATSUSHI NIKI ◽  
TADATAKA KOIDE ◽  
...  
Keyword(s):  
Insulin Release ◽  
Voltage Dependent ◽  
Stimulation Of

scholarly journals Stimulation of protein kinase C and insulin release by 1-oleoyl-2-acetyl-glycerol

1985 ◽  
Vol 149 (1) ◽  
pp. 23-27 ◽  
Author(s):  
Willy J. MALAISSE ◽  
Marjorie E. DUNLOP ◽  
Paulo C. F. MATHIAS ◽  
Francine MALAISSE-LAGAE ◽  
Abdullah SENER
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Insulin Release ◽  
Kinase C ◽  
Stimulation Of

Effects of l-leucine, its 2-keto acid metabolite and its nonmetabolized analogue on rat tumoral islet cell function

1988 ◽  
Vol 1 (1) ◽  
pp. 69-76 ◽  
Author(s):  
V. Leclercq-Meyer ◽  
J. Marchand ◽  
A. Sener ◽  
F. Blachier ◽  
W. J. Malaisse
Keyword(s):  
Insulin Release ◽  
Cell Function ◽  
Islet Cells ◽  
Adenine Nucleotides ◽  
Secretory Response ◽  
Acid Metabolite ◽  
Dual Effect ◽  
Islet Cell Function ◽  
Insulinoma Cells ◽  
Stimulation Of

ABSTRACT l-Leucine and 2-ketoisocaproate stimulated insulin release from perifused rat tumoral islet cells (RINm5F line). The secretory response coincided with an increase in the intracellular ATP/ADP ratio, a stimulation of 45Ca outflow from cells perifused in the presence of extracellular Ca2+, and an increase in 32P efflux from cells prelabelled with radioactive orthophosphate. In contrast to d-glucose, however, l-leucine or 2-ketoisocaproate failed to decrease 86Rb outflow, to inhibit 45Ca outflow from cells perifused in the absence of Ca2+ and to enhance the labelling of inositol-containing phospholipids in cells exposed to myo-[2-3H]inositol. These findings suggest that d-glucose, l-leucine and 2-ketoisocaproate exert dissimilar effects on the subcellular distribution of adenine nucleotides and/or 86Rb. The nonmetabolized analogue of l-leucine, 2-aminobicyclo-[2.2.1]heptane-2-carboxylic acid (BCH), also caused an initial stimulation of insulin release and 32P efflux, but this was soon followed by a severe and irreversible inhibition of insulin output, associated with a permanent enhancement of 86Rb outflow. The dual ionic and secretory response to BCH is interpreted in the light of its dual effect on the catabolism of endogenous amino and fatty acids, and raises the view that BCH could be used to interfere with the function of insulinoma cells.

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