Abstract
Microdissected islets from obese-hyperglycemic mice were used to study the uptake, oxidation and insulin-releasing capacity of glutamic acid. Glutamic acid was taken up slowly by the islets, yielding distribution ratios around unity. The uptake of glutamic acid was depressed by alanine, whereas glucose had a minor stimulatory effect Glibenclamide, leucine, arginine or galactose had no effect on the uptake of glutamic acid. The low rate of oxidationof glutamic acid was substantially increased when glucose was added to the incubation medium. Glutamic acid did not stimulate insulin release regardless of whether glucose was present in the incubation medium. The data suggest that the pancreatic <i>β</i>-cells are equipped with membrane transport systems for glutamic acid which do not serve as trigger sites for insulin release.
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