Preservation of the anomeric specificity of glucose-induced insulin release in partially pancreatectomized rats

Summary Attenuation, suppression or even inversion of the normal preference of glucose-stimulated insulin release for the -anomer of the hexose was recently proposed to represent a feature of Beta-cell glucotoxicity in Type 2 (non-insulin-dependent) diabetes mellitus. Since recent reports emphasize the possible significance of Beta-cell secretory hyperactivity as a determinant of such a glucotoxicity, the anomeric specificity of glucose-induced insulin release was examined in normoglycaemic partially pancreatectomized rats. About 80–85% of the pancreas was removed, the animals then being given sucrose via their drinking water up to the time of killing. In these animals, -D-glucose was more efficient than -D-glucose in stimulating insulin release from the perfused pancreas, the / ratio in insulin output not being significantly different from that found in control rats. It is concluded, therefore, that the anomeric malaise, taken as a manifestation of Beta-cell glucotoxicity, it attributable to hyperglycaemia rather than to Beta-cell secretory hyperactivity.