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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Diabetes 1981 Jul
PMID:Intestinal sugar transport in experimental diabetes. 645

It was observed previously (Cs aky , T.Z. and Fischer, E. (1981) Diabetes 30, 568-574), that sustained hyperglycemia enhances the intestinal transport of aldohexoses ; on the other hand, hyperfructosemia affects primarily the transport of fructose. The present study examines in detail the hyperketosemia -induced intestinal ketose transport. Intravenously infused 3-O- methylfructose produces marked 3-O- methylfructosemia without concomitant hyperglycemia; in such animals the intestinal transport of both fructose and 3-O- methylfructose increased. The hyperketosemia -induced increased ketose transport was inhibited by phloretin but only if placed on the serosal compartment. Phlorizin affects neither the basal nor the induced intestinal ketohexose transport. The enhancement of the intestinal ketohexose transport is not sodium-dependent and is not inhibited by ouabain.
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PMID:Effects of ketohexosemia on the ketohexose transport in the small intestine of rats. 672 48