Cholecystokinin (CCK8) regulates glucagon, insulin, and somatostatin secretion from isolated rat pancreatic islets: interaction with glucose

1987 ◽  
Vol 410 (3) ◽  
pp. 284-287 ◽  
Author(s):  
E. J. Verspohl ◽  
H. P. T. Ammon
1992 ◽  
Vol 14 (2) ◽  
pp. 45-50 ◽  
Author(s):  
Barthold Vonen ◽  
Kjell Bertheussen ◽  
Anton K. Gi�ver ◽  
Jon Florholmen ◽  
Per G. Burhol

1992 ◽  
Vol 52 (2) ◽  
pp. 107-112 ◽  
Author(s):  
B. Vonen ◽  
J. Florholmen ◽  
D. Malm ◽  
P. Torjessen ◽  
P. G. Burhol

1999 ◽  
Vol 276 (1) ◽  
pp. E19-E24 ◽  
Author(s):  
Feng Wang ◽  
Thomas E. Adrian ◽  
Gunilla T. Westermark ◽  
Xianzhong Ding ◽  
Thomas Gasslander ◽  
...  

Islet amyloid polypeptide (IAPP, or amylin) is produced in pancreatic β-cells. The intraislet significance of IAPP is still uncertain. In the present study, paracrine effects of endogenous IAPP and somatostatin were investigated in isolated rat pancreatic islets. The intraislet IAPP activity was inhibited with an IAPP antiserum or a specific antagonist [IAPP-(8—37)]. Somatostatin activity was inhibited by immunoneutralization. Basal insulin and glucagon secretion were not affected by the somatostatin and/or IAPP blockade. Arginine-stimulated insulin and glucagon secretion were dose dependently increased by IAPP antiserum, IAPP-(8—37), and somatostatin antiserum, respectively. Arginine-stimulated somatostatin secretion was dose dependently potentiated by IAPP antiserum. Insulin secretion induced by 16.7 mM glucose was enhanced by IAPP antiserum and IAPP-(8—37), respectively. A combination of somatostatin antiserum with IAPP antiserum or IAPP-(8—37) further enhanced the arginine-stimulated insulin and glucagon secretion compared with effects when the blocking reagents were used individually. These results indicate that endogenously produced IAPP tonally inhibits stimulated insulin, glucagon, and somatostatin secretion. Furthermore, the paracrine effects of IAPP and somatostatin are additive.


1989 ◽  
Vol 49 (2) ◽  
pp. 139-143 ◽  
Author(s):  
B. Vonen ◽  
T. J. Florholmen ◽  
A. K. Giæver ◽  
P. Burhol

1991 ◽  
Vol 177 (3) ◽  
pp. 932-938 ◽  
Author(s):  
Carol L. Broderick ◽  
Gerald S. Brooke ◽  
Richard D. DiMarchi ◽  
Gerald Gold

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 ◽  
...  

1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp

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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