AJP - Endocrinology and Metabolism, Vol 238, Issue 2 96-103, Copyright © 1980 by American Physiological Society
Regulation of calcium fluxes in pancreatic islets: glucose-induced calcium-calcium exchange
A. Herchuelz, E. Couturier and W. J. Malaisse
Glucose provokes an initial fall followed by a secondary rise in 45Ca
efflux from prelabeled pancreatic islets. Prior exposure of the islets to
calcium-depleted media does not suppress the secondary rise, provided that
the extracellular calcium concentration is normalized 2 min before addition
of glucose. Such a treatment significantly reduces insulin release. The
secondary rise, as distinct from the initial fall, is inhibited under
conditions known to interfere with calcium entry into the beta-cell, e.g.,
in the presence of ruthenium red or cobalt. Calcium itself in high
concentrations provokes a dramatic increase in 45Ca efflux. The magnitude
of this calcium-induced efflux is enhanced by prior exposure of the islets
to calcium-depleted media. Imidazole and the theophylline do not modify the
effect of glucose on 45Ca efflux. It is proposed that the glucose-induced
secondary rise in 45Ca efflux corresponds to a calcium-calcium exchange
process in which influent 40Ca displaces 45Ca from intracellular sites.
