Inhibition of insulin release by alpha- and beta-D-galactose pentaacetate.

Several monosaccharide polyacetate esters display higher biological efficiency than the corresponding unesterified carbohydrates, this being attributable to their capacity to cross the plasma membrane without requiring the intervention of a specific carrier system and to their subsequent intracellular esterase-catalyzed hydrolysis. Some of these esters, however, also exert a direct effect upon a receptor system apparently displaying analogies with that involved in the identification of bitter compounds by taste buds. For instance, under suitable experimental conditions, esters of non-nutrient monosaccharides, such as L-glucose, D-mannoheptulose or 2-deoxy-D-glucose, unexpectedly stimulate insulin release. The present work reveals that alpha-D-galactose pentaacetate and, to a lesser extent, beta-D-galactose pentaacetate both inhibit leucine-induced insulin release in rat pancreatic islets. This indicates that the postulated receptor system displays anomeric specificity and may participate in a negative modulation of insulin secretion. It is proposed that advantage could be taken of the negative insulinotropic action of D-galactose pentaacetate esters to prevent excessive insulin release in pathological situations.