Noncarbohydrate nutrients such as 2-ketoisocaproate, L-glutamine, L-leucine and its nonmetabolized analog, beta-2-aminobicyclo[2,2,1]heptane-2-carboxylic acid (BCH) were able to mimic, to a limited extent, the protective action of D-glucose against the inhibitory effect of alloxan on glucose-stimulated insulin release. L-glutamine potentiated the protective action of BCH but not that of 2-ketoisocaproate or L-leucine. These data lend support to the view that the cytotoxic effect of alloxan is linked to the generation of peroxide. Agents which stimulate islet metabolism may protect against such a cytotoxic effect by increasing the production rate of reducing equivalents in the islet cells.
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Sener et al. (1982) studied this question.
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