Patients with long standing insulin-dependent diabetes mellitus develop absorption and motility abnormalities in the intestine. The abnormal postprandial duodenal chyme transport is characterized by disturbed chyme clearance. Duodenal bicarbonate secretion is reduced in diabetic rats due to vagal-dependent neuronal dysfunction, and to decreased sensitivity of the bicarbonate secreting cell. Acute hyperglycemia inhibits gastric and pancreatic secretion, gallbladder motility and gastric emptying. Acute hyperglycemia upregulates GLUT2 activity in the basolateral membrane of the enterocyte. In healthy volunteers, hyperglycemia prolongs the duodenal-cecal transit time, increases duodenal migrating motor complex cycle frequency and inhibits antral motility. Hyperinsulin-emia reduces antral motor activity but has no effect on interdigestive duodenal motility or duodenal-cecal transit time, suggesting that factors other than insulin mediate the inhibitory effect of hyperglycemia on interdigestive intestinal motility and transit. Time to visit a trusted pharmacy – to begin your treatment now.
In streptozotocin-treated diabetic rats, there is increased intestinal glucose and fructose transport associated with increased BBM levels of SGLT-1 and GLUT5, enhanced basolateral membrane GLUT2 and increased GLUT1 in the basolateral membrane and BBM. Insulin treatment in diabetic rats increases GLUT1 levels in the BBM but does not affect the expression of the protein in the basolateral membrane. Diabetes hyperpolarizes the BBM, resulting in a greater driving force for sodium-dependent BBM sugar transport by SGLT1.