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.

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