Abstract

Evidence has been published that L-alanine may, under appropriate conditions, promote insulin secretion in normal rodent islets and various beta cell lines. Previous results utilising the clonal beta-cell line BRIN-BD11, demonstrated that alanine dramatically elevated insulin release by a mechanism requiring oxidative metabolism. We demonstrate in this paper that addition Of L-alanine had an insulinotropic effect in dispersed primary islet cells. Addition Of D-glucose increased L-alanine consumption in both BRIN-BD11 cells and primary islet cells. L-glutamine consumption in the BRIN-BD11 cell line and primary rat islets was also determined. The consumption rate was in line with that previously reported for cells of the immune system and other glutamine-utilising cells or tissues. However, L-alanine consumption was at least an order of magnitude higher than L-glutamine consumption. The metabolism Of L-alanine in the beta-cell may result in stimulation of insulin secretion via generation of metabolic stimulus secretion coupling factors such as L-glutamate.