GLUT2 is a facilitative glucose transporter in the liver, pancreas, intestine, kidney and brain. Because it is a low-affinity and high-capacity transporter, GLUT2 transports dietary sugars like glucose, fructose and galactose in a wide range of physiological concentrations to ensure large bidirectional fluxes of sugars in and out cells. In the intestine, GLUT2 is a major contributor to sugar efflux from the cell through the basolateral side of enterocytes into the blood stream. In the past decade, the understanding of the role of GLUT2 has been improved and this facilitative transporter can now be considered a key element for the control of sugar absorption in the course of a meal. The acute regulation of the location of GLUT2 in enterocytes relies on the presence of sufficiently high concentrations of monosaccharides in the lumen of the small intestine to trigger, within minutes, the translocation of GLUT2 into the apical membrane. This high capacity pathway of sugar transport through enterocytes provides a major route of absorption when dietary sugars are abundant; it has been described in species from insects to mammals. The translocation of GLUT2 is also a target for nutrient sensing mechanisms, among which one can distinguish intestinal sweet taste receptor activation by natural and artificial sweeteners, and hormone signalling especially insulin and GLP-2. Inhibition of sugar absorption by insulin release from the pancreas may be important in the control of glucose homeostasis in the postprandial state and indeed insulin internalizes GLUT2 from the apical membrane back into intracellular vesicles. The contribution of GLUT2 to metabolic diseases previously appeared modest. However, permanent apical GLUT2, increasing the absorption capacity for sugar, is found in experimental diabetes and insulin resistance induced by an excess of sugar and fat in the diet. In obese patients, we found GLUT2 located in the apical membrane of enterocytes even after an overnight fast. Thus the regulation of apical and basolateral location of GLUT2 is profoundly altered in these patients and this might be an issue in the context of overweight and metabolic management of obesity.