Mechanism of action of glucagon-like peptide-17–36NH2 in isolated rat pancreatic islets and abrogation of its effects in long-term incubations

Endocrine ◽  
1995 ◽  
Vol 3 (11) ◽  
pp. 795-799 ◽  
Author(s):  
K. A. Gronau ◽  
P. L. Brubaker
Keyword(s):  
Pancreatic Islets ◽  
Mechanism Of Action ◽  
Rat Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Isolated Rat

Human and rat amylin have no effects on insulin secretion in isolated rat pancreatic islets

1991 ◽  
Vol 177 (3) ◽  
pp. 932-938 ◽  
Author(s):  
Carol L. Broderick ◽  
Gerald S. Brooke ◽  
Richard D. DiMarchi ◽  
Gerald Gold
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Rat Pancreatic Islets ◽  
Isolated Rat

Angiotensin II induces superoxide generation via NAD(P)H oxidase activation in isolated rat pancreatic islets

2009 ◽  
Vol 153 (1-3) ◽  
pp. 1-6 ◽  
Author(s):  
A.E. Hirata ◽  
D. Morgan ◽  
H.R. Oliveira-Emilio ◽  
M.S. Rocha ◽  
C.R.O. Carvalho ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pancreatic Islets ◽  
Superoxide Generation ◽  
Rat Pancreatic Islets ◽  
Isolated Rat

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.

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