Noncarbohydrate nutrients protect against alloxan-induced inhibition of insulin release.
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.
D000496:Alloxan / Q000494:pharmacology*; D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D005947:Glucose / Q000378:metabolism; D005973:Glutamine / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D007515:Islets of Langerhans / Q000187:drug effects*; D007651:Keto Acids / Q000494:pharmacology*; D007930:Leucine / Q000494:pharmacology; D009243:NAD / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D051381:Rats; D013997:Time Factors
D000596:Amino Acids; D007328:Insulin; D007651:Keto Acids; D005973:Glutamine; D009243:NAD; D009249:NADP; D000496:Alloxan; C013082:alpha-ketoisocaproic acid; D007930:Leucine; D005947:Glucose