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An unmetabolizable synthetic amino acid, 2-aminobicyclo2,2,1-heptane-2-carboxylic acid (BCH), leucine, arginine and glucose were administered intravenously to 3 dogs. Chlorpropamide, mannoheptulose and diazoxide were administered before or concomitantly with some of these infusions. BCH induced significant increases in plasma insulin in the chlorpropamide-pretreyted dogs. Insulin release induced by BCH, as well as that by leucine, is (a) accentuated by chlorpropamide, (b) increased or unaffected by mannoheptulose and (c) inhibited by diazoxide. Arginine-induced insulin release is suppressed completely by mannoheptulose. Neither leucine nor BCH increased plasma levels of glucagon. The results of these studies: 1) indicate that BCH is a functional leucine analogue with respect to pancreatic islet cell function, 2) provide direct evidence that amino acids themselves rather than one of their metabolites stimulate insulin release, 3) suggest that the beta cell receptor for stimulation of insulin release by the unmetabolizable amino acid BCH (and leucine) may be a transport receptor site, and 4) provide further evidence that the mechanism by which leucine (and BCH) induce insulin release differs from that by which arginine induces the release of insulin.
Fajans et al. (1971) studied this question.