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).