Effect of Anomers of D-Mannose on Insulin Release from Perfused Rat Pancreas*

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Abstract
The α-anomer of D-glucose was found to produce a greater insulin release than the β-anomer. This was interpreted as a direct action of the glucose molecule on a glucoreceptor. However, an alternative explanation for this was proposed, based on the recent demonstration that islet glucose metabolism favored the a-anomer because of the stereospecificity of phosphoglucose isomerase for α-glucose-6-phosphate. Since phosphomannose isomerase is known to be stereospecific for β-mannose- 6-phosphate, we have compared the effects of the α- and β- anomers of D-mannose on insulin release in the isolated perfused rat pancreas. With a concentration less than 1.5 mg/ml, neither anomer of D-mannose significantly stimulated insulin release; however, at concentrations of 2 and 3 mg/ml, the α-anomer was more potent than the β-anomer in stimulating insulin release. The effects of the two anomers were not significantly different at a concentration of 5 mg/ml. a-Anomeric stereospecificity was equally demonstrable in both phases of insulin release. A dominant stimulatory effect of the a-anomer over the β-anomer in lower concentrations was observed in mannose-induced insulin release, as was previously noted using D-glucose, despite the opposite anomeric specificities of the isomerases for glucose-6-phosphate and mannose-6-phosphate. The data suggest that pancreatic B-cells identify the a-anomer of hexoses as the dominant stimulus for insulin release at the level before the phosphohexose isomerase step, most probably at a receptor site(s) of the cell membrane.