A high affinity glutamate/aspartate transport system in pancreatic islets of Langerhans modulates glucose-stimulated insulin secretion.

The Journal of Biological Chemistry
C D WeaverT A Verdoorn

Abstract

To examine the role of glutamatergic signaling in the function of pancreatic islets, we have characterized a high affinity glutamate/aspartate uptake system in this tissue. The islet [3H]glutamate uptake activity was Na(+)-dependent, and it was blocked by L-trans-pyrrolidine-2,4-dicarboxylic acid, a blocker of neuronal and glial glutamate transporters. Islet glutamate transport activity exhibited a Vmax of 8.48 +/- 1.47 fmol/min/islet (n = 4), which corresponds to 102.2 +/- 17.7 pmol/min/mg islet protein. The apparent Km of islet glutamate transport activity depended on the glucose concentration used in the assay. In the presence of glucose concentrations that do not stimulate insulin secretion (2.8 mM), the apparent Km was 34.7 +/- 7.8 microM (n = 3). However, in high glucose (16.7 mM) the apparent Km increased to 112.7 +/- 16.5 microM (n = 3) with little or no change in Vmax. Like most known plasma membrane glutamate transporters, islet glutamate transporters also transported D-aspartate. Anti-D-aspartate immunoreactivity showed that the islet glutamate/aspartate transport activity was localized to the non-beta cell islet mantle. In perifusion experiments with isolated islets in the absence of exogenous amino acids, L-trans-p...Continue Reading

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