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Papers In Press, published online ahead of print August 30, 2000
Childrens Diabetes Center, University of Wisconsin Medical School, Madison, WI 53706
Corresponding Author: mjmacdon{at}facstaff.wisc.edu
Experiments do not support a recent claim that glutamate formed from the amination of citric acid cycle derived
J. Biol. Chem, 10.1074/jbc.C000411200
Submitted on June 27, 2000
Revised on August 4, 2000
Accepted on August 29, 2000
Glutamate is not a messenger In insulin secretion
-ketoglutarate is a messenger in glucose-induced insulin secretion (P. Maechler and C. Wollheim, Nature 402: 685-689, 1999). Glucose, leucine, succinic acid methyl ester and -ketoisocaproic acid all markedly stimulate insulin release, but do not increase glutamate levels in pancreatic islets. Increasing the intracellular glutamate levels to 10 fold higher than basal levels by adding glutamine to islets does not stimulate insulin release. When leucine is applied to islets in addition to glutamine, insulin release is almost as high as with glucose alone. This is consistent with the known ability of leucine to allosterically activate glutamate deamination by glutamate dehydrogenase which can supply -ketoglutarate to the citric acid cycle. Experiments with mitochondria from pancreatic islets suggest that flux through the glutamate dehydrogenase reaction is quiescent during glucose-induced insulin secretion. These experiments support the traditional idea that when insulin release is associated with flux through glutamate dehydrogenase, the flux is in the direction of -ketoglutarate.
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