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Am J Physiol Endocrinol Metab 257: E473-E478, 1989;
0193-1849/89 $5.00
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AJP - Endocrinology and Metabolism, Vol 257, Issue 4 E473-E478, Copyright © 1989 by American Physiological Society

ARTICLES

Membrane and intracellular effects of adenosine in mouse pancreatic beta-cells

G. Bertrand, P. Petit, M. Bozem and J. C. Henquin
Unite de Diabetologie et Nutrition, University of Louvain Faculty of Medicine, Brussels, Belgium.

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.


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