Further Studies on the Relationship between Insulin Release and Lanthanum-Nondisplaceable45Ca2+Uptake by Pancreatic Islets: Effects of Fructose and Starvation*

Abstract

Relationships between the release of insulin and the incorporation of 45Ca2+ into a La-nondisplaceable (intracellular) pool were studied in islets microdissected from the pancreatic glands of non-inbred ob/ob mice. In comparison with D-glucose, D-fructose was slowly oxidized and had only marginal effects on insulin release. However, fructose was as effective as glucose in stimulating the La-non-displaceable 45Ca2+ uptake. The 45Ca2+ uptake was dose-dependent on the concentration of fructose in the range 0-20 mM; the mM; the same dose-dependence was obtained with glucose. Fasting the mice for 3 days caused a total block of the insulin secretory response to 20 mM glucose, but it produced an enhancement of the glucose-induced 45Ca2+ uptake. Both the inhibition of insulin release and the enhancement of 45Ca2+ uptake were counteracted by pretreating the isolated islets with 20-40 mM D-glucose; pretreatment with L-glucose or fructose could not counteract the effects of fasting. Although some functional relationship may exist between the La-nondisplaceable uptake of 45Ca2+ and the insulin secretory apparatus, the uptake of Ca2+ is not simply the result of stimulated insulin release.