Failure of glucose to affect 86rubidium efflux and 45calcium uptake of fetal rat pancreatic islets.

Ion movements and insulin secretion of pancreatic islets of adult and fetal rats have been studied at three glucose concentrations. In islets of adult rats, 86Rb efflux is maximally decreased by 5.6 mM-glucose. 16.7 mM-glucose caused a biphasic efflux pattern which may be due to glucose-stimulated Ca uptake. In islets of fetal rats elevation of the glucose concentration from 3 to 5.6 or 16.7 mM does not cause a change of 86Rb efflux, and the fractional efflux from fetal islets in the presence of 3 mM-glucose is similar to that from adult rat islets in the presence of 5.6 mM-glucose. Elevation of the glucose concentration from 3 to 16.7 mM is not associated with an increase in 45Ca uptake into fetal islets, although this change in glucose concentration doubles 45Ca uptake into adult islets. When challenged with 16.7 mM-glucose, fetal islets exhibit no insulin secretory response; however, they do respond to theophylline. It is concluded that the failure of fetal islets to exhibit an insulin-secretory response when challenged with glucose might be related to the inability of glucose to affect 86Rb efflux and Ca uptake. The present data are discussed in light of differences between pancreatic islets of fetal and adult rats with respect to the redox state of pyridine nucleotides, thiols and glucose metabolism.