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1. The release of 45calcium from prelabelled pancreatic islets is rapidly and almost totally inhibited by lanthanum. 2. Glucose provokes an intitial fall followed by a secondary rise in 45calcium efflux. The latter rise occurs concomitantly with insulin release. Its magnitude is reduced whenever the secretory response to glucose is inhibited, e.g. in the absence of extracellular calcium, presence of Verapamil, or at high magnesium concentration. 3. However, under suitable conditions, the glucose-induced secondary rise in 45calcium efflux is not totally suppressed whilst insulin release is totally abolished. 4. Inversely, when calcium is replaced by barium in the perifusate, glucose increases insulin output without causing any obvious secondary rise in 45calcium efflux. 5. It is concluded that this secondary rise, which originates from a lanthanum-nondisplaceable calcium pool, does not correspond solely to an exocytotic release of 45calcium. It could represent, in part at least, a displacement of 45calcium from cellular sites and reflect a glucose-induced increase in the rate of calcium entry in islet cells.

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				W. J. Malaisse, L. C. Best, A. Herchuelz, M. Hiriart, H. Jijakli, M. M. Kadiata, E. Larrieta-Carasco, A. Laghmich, K. Louchami, D. Mercan, et al. Insulinotropic action of beta -L-glucose pentaacetate Am J Physiol Endocrinol Metab, December 1, 1998; 275(6): E993 - E1006. [Abstract] [Full Text] [PDF]