Does leucine- and norleucine-induced insulin release depend on amino acid aminotransferase activity?
In the absence of another exogenous nutrient, L-leucine but not L-norleucine stimulates insulin release from rat pancreatic islets, although the corresponding keto acids, 2-ketoisocaproate and 2-ketocaproate, are equally potent secretagogues. Such a situation cannot be ascribed to the preferential transamination of L-leucine as compared to L-norleucine in islet homogenates. Indeed, in the presence of a suitable activator of glutamate dehydrogenase, L-leucine and L-norleucine stimulate secretion to the same extent. It is concluded that the rate of transamination of these amino acids in intact islet cells depends on the availability of a 2-keto acid partner rather than on the assayed amino acid aminotransferase activity.
D000596:Amino Acids / Q000494:pharmacology; D000614:Aminocaproates / Q000494:pharmacology*; D000818:Animals; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D007651:Keto Acids / Q000494:pharmacology; D007930:Leucine / Q000494:pharmacology*; D009646:Norleucine / Q000494:pharmacology*; D051381:Rats; D013329:Structure-Activity Relationship; D000637:Transaminases / Q000378:metabolism*
D000596:Amino Acids; D000614:Aminocaproates; D007328:Insulin; D007651:Keto Acids; D009646:Norleucine; D000637:Transaminases; D007930:Leucine