Electrical activity and insulin release in pancreatic beta cells

1988 ◽  
Vol 90 (1-2) ◽  
pp. 127-138 ◽  
Author(s):  
Joel Keizer
1989 ◽  
Vol 257 (4) ◽  
pp. E473-E478 ◽  
Author(s):  
G. Bertrand ◽  
P. Petit ◽  
M. Bozem ◽  
J. C. Henquin

Mouse islets were used to study the effects of adenosine and its stable analogue L-N6-phenylisopropyladenosine (L-PIA) on pancreatic beta-cell function. At a high concentration (500 microM), adenosine augmented glucose-induced electrical activity in beta-cells and potentiated insulin release. These effects were prevented by the inhibitor of nucleoside transport nitrobenzylthioguanosine. They probably result from the metabolism of adenosine by beta-cells. At a lower concentration (50 microM), adenosine caused a small and transient inhibition of glucose-induced electrical activity and insulin release. L-PIA (10 microM) slightly and transiently inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. When adenylate cyclase was stimulated by forskolin in the presence of 15 mM glucose, insulin release was strongly augmented. Under these conditions, L-PIA and adenosine (with nitrobenzylthioguanosine) caused a sustained inhibition. No such inhibition was observed when insulin release was potentiated by dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). These data are consistent with the existence of A1 purinergic receptors on mouse beta-cells. They could mainly serve to attenuate the amplification of insulin release brought about by agents acting via cAMP.


1981 ◽  
Vol 240 (3) ◽  
pp. C116-C120 ◽  
Author(s):  
M. S. Sheppard ◽  
P. Meda

Gap junctions between pancreatic beta-cells were quantitatively assessed in freeze-fracture replicas of isolated rat islets of Langerhans incubated for 90 min with or without the potassium conductance blocker tetraethylammonium (TEA). The results show that TEA increases the median number of particles per beta-cell gap junction but not the frequency of gap junctions at both nonstimulating and threshold-stimulating concentrations of glucose. TEA increased the relative gap junctional area at both concentrations of glucose. TEA had no effect on insulin release at a basal concentration of glucose but potentiated that release at the threshold glucose level. Thus TEA modifies beta-cell gap junctions independently of its effect on insulin release. However, the junctional changes observed were greater when insulin release was also elevated.


2015 ◽  
Vol 41 (4) ◽  
pp. S65 ◽  
Author(s):  
Ivan Mauricio Suarez Castellanos ◽  
Aleksandar Jeremic ◽  
Vesna Zderic

Diabetologia ◽  
2010 ◽  
Vol 53 (5) ◽  
pp. 924-936 ◽  
Author(s):  
G. Sun ◽  
A. I. Tarasov ◽  
J. McGinty ◽  
A. McDonald ◽  
G. da Silva Xavier ◽  
...  

Diabetologia ◽  
1994 ◽  
Vol 37 (S2) ◽  
pp. S11-S20 ◽  
Author(s):  
B. Hellman ◽  
E. Gylfe ◽  
P. Bergsten ◽  
E. Grapengiesser ◽  
P. E. Lund ◽  
...  

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