scholarly journals ATP-independent glucose stimulation of sphingosine kinase in rat pancreatic islets

2010 ◽  
Vol 51 (8) ◽  
pp. 2171-2180 ◽  
Author(s):  
L. D. Mastrandrea ◽  
S. M. Sessanna ◽  
A. Del Toro ◽  
S. G. Laychock
Keyword(s):  
Pancreatic Islets ◽  
Sphingosine Kinase ◽  
Glucose Stimulation ◽  
Rat Pancreatic Islets ◽  
Stimulation Of

Mechanisms of synergism between glucose and cAMP on stimulation of insulin release

1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Ringer Solution ◽  
Intracellular Camp ◽  
Cyclic Monophosphate ◽  
Rat Pancreatic Islets ◽  
Individual Effects ◽  
The Individual ◽  
Isolated Rat ◽  
Stimulation Of

The mechanism of synergism between glucose and adenosine 3',5'-cyclic monophosphate (cAMP) on insulin release has been studied. Synergism may result from 1) inhibition of Na+-Ca2+ exchange by glucose and 2) a cAMP-induced sensitization of the release machinery to Ca2+. To distinguish between these two possibilities, isolated rat pancreatic islets were perifused with agents that raise intracellular levels of cAMP [3-isobutyl-1-methylxanthine (IBMX) and forskolin] and others that increase intracellular concentrations of Ca2+ either by blocking Na2+-Ca2+ exchange (ouabain and choline-Ringer solution) or by causing increased Ca2+ influx (KCl, carbachol, and 10 mM Ca2+). The results indicate that both the combination of cAMP and increased Ca2+ influx or blocked Na2-Ca2+ exchange and increased Ca2+ influx potentiated insulin release. When the relative potentiating abilities of cAMP and blocked Na2+-Ca2+ exchange were compared by determining the individual effects of IBMX and 1 mM ouabain (a concentration that causes similar inhibition of 45C2+ efflux as 16.7 mM glucose) in the presence of carbachol, cAMP was only 1.4 times more potent as a potentiating agent than blocked Na+-Ca2+ exchange. The greatest potentiation of insulin release was observed when Na+-Ca2+ exchange was blocked in the presence of increased levels of intracellular cAMP.

Diazoxide unmasks glucose inhibition of insulin release by counteracting entry of Ca2+

1988 ◽  
Vol 255 (4) ◽  
pp. E422-E427 ◽  
Author(s):  
P. Bergsten ◽  
E. Gylfe ◽  
N. Wesslen ◽  
B. Hellman
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Secretory Response ◽  
Glucose Stimulation ◽  
Glucose Inhibition ◽  
Insulin Secretory Response ◽  
Stimulation Of

The interaction of diazoxide with the effects of glucose on the insulin-releasing mechanism was analyzed in beta-cell-rich pancreatic islets isolated from ob/ob mice. When added at a concentration of 400 microM to a medium containing 1.28 mM Ca2+, diazoxide converted glucose stimulation of insulin release into inhibition. Further addition of 2 mM theophylline restored the insulin secretory response to glucose. The paradoxical glucose inhibition of insulin release was accounted for by a diazoxide interaction with the entry of Ca2+, unmasking a capacity of the sugar to lower cytoplasmic Ca2+ below its resting concentration.

Stimulation of Biosynthetic Activity by Novel Succinate Esters in Rat Pancreatic Islets

1998 ◽  
Vol 55 (6) ◽  
pp. 909-913 ◽  
Author(s):  
Aouatif Laghmich ◽  
Laurence Ladrière ◽  
Francine Malaisse-Lagae ◽  
Heinz Dannacher ◽  
Fredrik Björkling ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Biosynthetic Activity ◽  
Rat Pancreatic Islets ◽  
Stimulation Of

Demonstration of glucose inhibition of insulin release in the presence of diazoxide

1987 ◽  
Vol 115 (2) ◽  
pp. 170-174 ◽  
Author(s):  
Peter Bergsten ◽  
Bo Hellman
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Β Cell ◽  
Glucose Stimulation ◽  
Inhibitory Component ◽  
Glucose Inhibition ◽  
Stimulation Of

Abstract. β-Cell-rich pancreatic islets from ob/ob mice were taken for measurements of insulin release in response to glucose after culture in RPMI 1640 medium. The stimulatory effect of 20 mmol/l glucose was converted into an inhibition when the medium was supplemented with 400 μmol/l diazoxide. Glucose inhibition of insulin release was observed when the islets had been cultured in the presence of 1 or 20 mmol/l glucose in media either containing or lacking Ca2+. The data provide further evidence for an inhibitory component in the action of glucose on insulin release, suggesting that glucose stimulation of the Ca2+ efflux is essential for the appearance of this inhibition.

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