L-Leucine and its nonmetabolized analog, 2-aminobicyclo-[2,2,1]heptane-2-carboxylic acid (BCH), do not act identically in pancreatic islets. For instance, BCH stimulates more markedly than leucine the output of 14 CO2 from islets prelabelled with L-[U-14C] glutamine. Although leucine and BCH stimulate insulin release to the same extent in the presence of glutamine, the rate of secretion is higher in leucine-stimulated than in BCH-stimulated islets when 2-ketoisocaproate is present in the incubation medium alone or together with glutamine. Such a difference in secretory rate coincides with contrasting effects of leucine and BCH, respectively, on both NH4+ production and glutamine oxidation by the islets exposed to 2-keto-isocaproate. These differences are best explained by the inability of BCH, as distinct from leucine, to act as a transamination partner of 2-ketoglutarate, and emphasize the view that the secretory response to nutrients tightly depends on the regulation of catabolic events in the islet cells.
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Şener et al. (1982) studied this question.