Intestinal sugar transport in experimental diabetes.

The increased sugar transport was examined in the isolated small intestine of streptozotocin-diabetic rats. In the small intestine of these animals, the rate of glucose absorption in vivo is slightly increased, but not that of galactose of 3-O-MG (3-O-Methylglucose); however, in the isolated small intestine, the mucosal-to-serosal but not the serosal-to-mucosal flux of glucose, galactose, and 3-O-MG is increased. The enhanced sugar transport is due neither to the direct toxic effect of streptozotocin nor to a lack of circulating insulin. It is not the result of an increased intraepithelial sugar metabolism. Hyperglycemia, produced gy i.v. glucose infusion, generates the same increase of the intestinal sugar transport as experimental diabetes but the high blood sugar has to be maintained for 4 h before the intestinal effect appears. Hyperglycemia and hypergalactosemia enhance the intestinal transport of glucose, galactose, and 3-O-MG, but not that of fructose; the transport of the latter is increased by hyperfructosemia. The enhanced intestinal sugar transport produced by high blood sugar inhibited by phloretin but not by phlorizin and is completely estimated in cycloheximide-treated animals. It is proposed that sustained high blood sugar induces the synthesis of new carrier sites which are most likely located in the basolateral membrane.