Hexoses are rapidly absorbed across the wall of the small intestine. Essentially all the hexoses are removed before the remains of a meal reach the terminal pa of the ileum. The sugar molecules pass from the mucosal cells to the blood in the capillaries draining into the poal vein. The transpo of most hexoses is dependent on Na+ in the intestinal lumen; a high concentration of Na+ on the mucosal surface of the cells facilitates and a low concentration inhibits sugar influx into the epithelial cells. This is because glucose and Na+share the same cotranspoer, or sympo, the sodium-dependent glucose transpoer (SGLT, Na+glucose cotranspoer). The members of this family of transpoers, SGLT 1 and SGLT 2, resemble the glucose transpoers responsible for facilitated diffusion in that they cross the cell membrane 12 times and have their -COOH and -NH2 terminals on the cytoplasmic side of the membrane. However, there is no homology to the glucose transpoer (GLUT) series of transpoers. SGLT-1 is responsible for uptake of dietary glucose from the gut. The related transpoer, SGLT 2, is responsible for glucose transpo out of the renal tubules. Because the intracellular Na+ concentration is low in intestinal cells as it is in other cells, Na+ moves into the cell along its concentration gradient. Glucose moves with the Na+ and is released in the cell. The Na+ is transpoed into the lateral intercellular spaces, and the glucose is transpoed by GLUT 2 into the interstitium and thence to the capillaries. Thus, glucose transpo is an example of secondary active transpo (see Chapter; the energy for glucose transpo is provided indirectly, by the active transpo of Na+out of the cell. This maintains the concentration gradient across the luminal border of the cell so that more Na+and consequently more glucose enter. When the Na+/glucose cotranspoer is congenitally defective, the resulting glucose/galactose malabsorption causes severe diarrhea that is often fatal if glucose and galactose are not promptly removed from the diet. SGLT-1 also transpos galactose, but fructose utilizes a different mechanism. Its absorption is independent of Na+ or the transpo of glucose and galactose; it is transpoed instead by facilitated diffusion from the intestinal lumen into the enterocytes by GLUT 5 and out of the enterocytes into the interstitium by GLUT 2. Some fructose is conveed to glucose in the mucosal cells. Insulin has little effect on intestinal transpo of sugars. In this respect, intestinal absorption resembles glucose reabsorption in the proximal convoluted tubules of the kidneys; neither process requires phosphorylation, and both are essentially normal in diabetes but are depressed by the drug phlorizin. The maximal rate of glucose absorption from the intestine is about 120 g/h.REF: GANONG&;S REVIEW OF MEDICAL PHYSIOLOGY, KIM BARRETT, HEDDWEN BROOKS, SCOTT BOITANO, SUSAN BARMANTWENTY THIRD EDITIONPAGE NO:453,454