The effects of D- and L-glyceraldehyde on glucose oxidation, insulin secretion and insulin biosynthesis by pancreatic islets of the rat.

D-glyceraldehyde stimulated insulin secretion from isolated rat pancreatic islets in static incubation and perifusion systems. At low concentrations (2-4 mM) D-glyceraldehyde was a more potent secretagogue than glucose. The insulinotropic action of 15 mM D-glyceraldehyde was not affected by D-mannoheptulose, was potentiated by cytochalasin B (5 mug/ml) and theophylline (4 mM), and was inhibited by both adrenalin (2 muM) and somatostatin (10 mug/ml). D-glyceraldehyde at a concentration of 1.5 mM produced a 10-fold increase of L-[4,5-3H]leucine incorporation into proinsulin and insulin without a significant increase into other islet proteins. Glucose at 1.5 mM did not stimulate proinsulin biosynthesis. D-Glyceraldehyde at concentrations higher than 1.5 mM, in marked contrast to glucose, progressively inhibited incorporation of labelled leucine into proinsulin + insulin and other islet proteins. D-Glyceraldehyde also inhibited the oxidation of glucose. L-Glyceraldehyde did not stimulate proinsulin biosynthesis and had less effect than the D-isomer on insulin release and glucose oxidation. The results strongly suggest that metabolites below D-glyceraldehyde-3-P are signals for insulin biosynthesis and release. Interaction of D-glyceraldehyde with a "membrane receptor" cannot, however, be excluded with certainty.