Membrane-transport of sugars in diabetes mellitus.

The transport of sugars in the isolated small intestine of diabetic rats was examined. It was found earlier (Csaky and Fischer 1981 and 1984) that one symptom of the diabetes, hyperglycemia, sustained for at least 4 hours, causes a marked enhancement of the mucosal-to-serosal flux of glucose, galactose and 3-0-methylglucose. Based on the finding that the enhanced sugar flux was inhibited by phloretin but not by phlorizin and was completely abolished by the protein-synthesis inhibitor, cycloheximide, the theory was proposed that sustained maintenance of high blood sugar induces the synthesis of new sugar carrier sites which are mostly likely localized in the basolateral membrane. In the present study it was found that sustained hyperglycemia significantly enhances the mucosal-to-serosal flux of 2-deoxy-glucose (2DG) but does not alter the flux of alpha-methylglucoside (alpha MG). As it is known that in the small intestine alpha MG is preferentially transported in the brush border while 2DG is a preferred substrate for the basolateral membrane, the present findings corroborate the theory that the enhancement of the intestinal sugar transport produced by sustained hyperglycemia is localized in the basolateral membrane. A working hypothesis is proposed that the high blood sugar sensing receptor localized in the basolateral membrane is identical with the transport receptor (carrier).