Effects of tetracaine on insulin release and calcium handling by rat pancreatic islets

1987 ◽  
Vol 252 (6) ◽  
pp. E727-E733
Author(s):  
S. M. el Motal ◽  
M. C. Pian-Smith ◽  
G. W. Sharp
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Culture Conditions ◽  
Isolated Islets ◽  
Calcium Handling ◽  
Ca Channels ◽  
Rat Pancreatic Islets ◽  
Voltage Dependent ◽  
Stimulate Insulin Release

The effects of tetracaine on insulin release and 45Ca2+ handling by rat pancreatic islets have been studied under basal (2.8 mM glucose), glucose-stimulated (5.6, 8.3, and 16.7 mM glucose), and 3-isobutyl-1-methylxanthine (IBMX)-stimulated conditions. Islets were isolated by the use of collagenase and used either directly (freshly isolated islets) or after a period under tissue culture conditions. Tetracaine was found to stimulate insulin release under basal conditions, to inhibit glucose-stimulated insulin release, and to potentiate insulin release stimulated by IBMX. In studies on the mechanisms underlying these effects, tetracaine was found to decrease glucose-stimulated net retention of 45Ca2+ (by an action to block the voltage-dependent Ca channels) and to mobilize Ca2+ from intracellular stores. These two actions form the basis for the inhibition of glucose-stimulated insulin release, which depends heavily on Ca2+ entry via the voltage-dependent channels and the synergism with IBMX to potentiate release. No inhibition of IBMX-stimulated release occurs because IBMX does not use the voltage-dependent channels to raise intracellular Ca2+.

Novel effects of insulin secretagogues on capacitation of insulin release and survival of cultured pancreatic islets

1990 ◽  
Vol 259 (4) ◽  
pp. E548-E554 ◽  
Author(s):  
M. J. MacDonald ◽  
L. A. Fahien ◽  
D. I. McKenzie ◽  
S. M. Moran
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Metabolic Pathways ◽  
Time Course ◽  
Reciprocal Relationship ◽  
Insulin Secretagogues ◽  
Low Glucose ◽  
Islet Survival ◽  
Stimulate Insulin Release

Agents that stimulate insulin release from fresh pancreatic islets were tested for their ability to capacitate pancreatic islets to secrete insulin and to support beta-cell survival in tissue culture. Capacitation was defined as the ability to release insulin after 24 h in culture in the presence of an insulinotropic concentration of a secretagogue. Viable islets that lose glucose-induced insulin release gradually regain it during culture for 24 h in 20 mM glucose. Survival was defined as the ability to regain glucose-induced insulin release. To measure insulin release after culture, islets were incubated with various secretagogues in Krebs-Ringer buffer for 1 h. Examples of the diverse patterns of responses included the following. Glucose was the only secretagogue that capacitated glucose-induced release. Leucine-, leucine plus glutamine-, and glyceraldehyde-induced release remained capacitated after culture with no secretagogue. Culture at high glucose completely inhibited leucine-induced release. Culture at low glucose (1 mM) or at both high leucine and glutamine abolished glucose-induced release. Only leucine and glutamine capacitated monomethyl succinate-induced release. All agents including subinsulinotropic glucose (1 mM), except D-glyceraldehyde, permitted islet survival. Thus the metabolic pathways for initiation, capacitation, and survival are not identical between and within secretagogues. There is a reciprocal relationship between leucine and glucose with respect to capacitation. Capacitation follows a time course, which suggests that it is regulated by enzyme induction.

Relation of Insulin Release to Cyclic AMP Content in Rat Pancreatic Islets Maintained in Tissue Culture

Diabetes ◽  
1978 ◽  
Vol 27 (7) ◽  
pp. 766-773 ◽  
Author(s):  
A. Rabinovitch ◽  
G. S. Cuendet ◽  
G. W. G. Sharp ◽  
A. E. Renold ◽  
D. H. Mintz
Keyword(s):  
Tissue Culture ◽  
Cyclic Amp ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets

scholarly journals Somatostatin- and Epinephrine-Induced Modifications of 45Ca++ Fluxes and Insulin Release in Rat Pancreatic Islets Maintained in Tissue Culture

1977 ◽  
Vol 60 (5) ◽  
pp. 1165-1173 ◽  
Author(s):  
Claes B. Wollheim ◽  
Masatoshi Kikuchi ◽  
Albert E. Renold ◽  
Geoffrey W. G. Sharp
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets ◽  
45Ca Fluxes

Interactions of Ca2+, Mg2+, and Na+ in regulation of insulin release from rat islets

1983 ◽  
Vol 244 (3) ◽  
pp. E222-E229
Author(s):  
D. Janjic ◽  
C. B. Wollheim
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Cellular Calcium ◽  
Rat Islets ◽  
Rat Pancreatic Islets ◽  
Strict Interpretation ◽  
Stimulate Insulin Release

The effects of glucose and ionic modifications on unidirectional Ca2+ efflux and insulin release has been studied. Rat pancreatic islets were isotopically equilibrated with 45Ca2+ for 2 days and then perifused at 10(-8) M Ca2+ to allow for strict interpretation of 45Ca2+ efflux. Under these conditions 16.7 mM glucose inhibited Ca2+ efflux but did not stimulate insulin release. Removal of Mg2+ from the buffer markedly stimulated Ca2+ efflux that was counteracted by glucose. The omission of Na+ decreased basal Ca2+ efflux by 30% at 10(-8) M Ca2+, thus demonstrating the importance of Na-Ca countertransport for Ca2+ extrusion. Like glucose, Na+ omission or the addition of ouabain attenuated Ca2+ efflux stimulated by Mg2+ removal. Glucose may interfere with Na-Ca countertransport because the actions of 16.7 mM glucose and Na+ omission were not additive. At 10(-8) M Ca2+, glucose elicited insulin release only when both 1) loss of cellular calcium was minimized by prior inhibition of Ca2+ efflux (Na+ omission or ouabain), and 2) Ca2+ mobilization was favored by Mg2+ removal. Under these conditions (in contrast to normal Ca2+), insulin release was not accompanied by increased Ca2+ efflux. Thus, unidirectional Ca2+ measurements do not permit the detection of Ca2+ mobilization in intact islets because glucose may concomitantly inhibit Ca2+ extrusion.

Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets

2000 ◽  
Vol 23 (4) ◽  
pp. 240-245 ◽  
Author(s):  
E. De Carlo ◽  
A. Milanesi ◽  
C. Martini ◽  
P. Maffei ◽  
N. Sicolo ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Endothelin 1 ◽  
Rat Pancreatic Islets ◽  
Endothelin 3 ◽  
Stimulate Insulin Release ◽  
Isolated Rat

scholarly journals Defective calcium handling and insulin release in islets from diabetic Chinese hamsters

1979 ◽  
Vol 180 (1) ◽  
pp. 233-236 ◽  
Author(s):  
E G Siegel ◽  
C B Wollheim ◽  
G W Sharp ◽  
L Herberg ◽  
A E Renold
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Chinese Hamster ◽  
Calcium Handling ◽  
Biphasic Insulin ◽  
Chinese Hamsters ◽  
Diabetic Chinese Hamsters ◽  
Biphasic Insulin Release

In pancreatic islets from normal Chinese hamsters preloaded with 45Ca2+, glucose-induced biphasic insulin release was associated with increased 45Ca2+ efflux; islets from diabetic hamsters showed decreased insulin release and no increase in 45Ca2+ efflux. The lack of stimulated 45Ca2+ efflux persisted even when glucose-induced insulin release was potentiated by 3-isobutyl-1-methylxanthine. Since glucose-stimulated 45Ca2+ uptake by diabetic islets was not impaired, a defect in intracellular Ca2+ handling may be involved in the defective insulin release of the diabetic Chinese hamster.

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