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L-Leucine and 2-ketoisocaproate stimulated insulin release from perifused rat tumoral islet cells (RINm5F line). The secretory response coincided with an increase in the intracellular ATP/ADP ratio, a stimulation of ⁴⁵Ca outflow from cells perifused in the presence of extracellular Ca²⁺, and an increase in ³²P efflux from cells prelabelled with radioactive orthophosphate. In contrast to D-glucose, however, L-leucine or 2-ketoisocaproate failed to decrease ⁸⁶Rb outflow, to inhibit ⁴⁵Ca outflow from cells perifused in the absence of Ca²⁺ and to enhance the labelling of inositol-containing phospholipids in cells exposed to myo-[2-³H]inositol. These findings suggest that D-glucose, L-leucine and 2-ketoisocaproate exert dissimilar effects on the subcellular distribution of adenine nucleotides and/or ⁸⁶Rb. The nonmetabolized analogue of L-leucine, 2-aminobicyclo-[2.2.1]heptane-2-carboxylic acid (BCH), also caused an initial stimulation of insulin release and ³²P efflux, but this was soon followed by a severe and irreversible inhibition of insulin output, associated with a permanent enhancement of ⁸⁶Rb outflow. The dual ionic and secretory response to BCH is interpreted in the light of its dual effect on the catabolism of endogenous amino and fatty acids, and raises the view that BCH could be used to interfere with the function of insulinoma cells.