Transport and oxidation of glycine in mammalian pancreatic islets with reference to the mechanism of amino acid-induced insulin release.

Abstract

Microdissected pancreatic islets of obese-hyperglycemic mice were used for studying the uptake, oxidation and insulin-releasing ability of glycine. Glycine did not influence insulin release either in the presence or absence of glucose. It was rapidly taken up by the islet cells, reaching distribution ratios much higher than unity. This concentrative uptake was depressed by the omission of sodium from the medium. L-Alanine, L-leucine, D-glucose, or glibenclamide also reduced the glycine uptake, whereas diazoxide had no effect. The production of radioactive CO<sub>2</sub> from uniformly <sup>14</sup>C-labeled glycine remained insignificant even when tested at concentrations as high as 20 mM. It is suggested that the <i>β</i>-cells transport glycine by the alanine-preferring A-system. The data are consistent with our previous concept that this system does not represent a trigger site for insulin release from mature mouse-<i>β</i>-cells. Glycine appears to be of minor importance as a fuel for the <i>β</i>-cells.