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Intestinal sugar absorption refers to the process by which dietary monosaccharides—primarily glucose, galactose, and fructose—are transported across the intestinal epithelium into the bloodstream. The classic model describes SGLT1 as the major apical (brush-border) Na^+/glucose cotransporter responsible for active glucose and galactose uptake, while GLUT5 mediates fructose absorption. GLUT2 is conventionally the basolateral transporter for exit into blood, but at high luminal glucose/fructose loads, GLUT2 can translocate to the apical membrane, enabling facilitated diffusion and accelerating absorption. These pathways are upregulated in diabetes, contributing to hyperglycemia and have become targets for experimental pharmacological intervention[1][2][3][4][5].
Inhibition of SGLT1 decreases glucose uptake in the small intestine, lowering postprandial blood sugar\nInhibition of GLUT2 may limit bulk glucose and fructose absorption at high luminal concentrations
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