Metformin is an anti-diabetic drug widely used to treat type 2 diabetes mellitus. Several studies have demonstrated that in vivo, metformin decreases both hepatic glucose production and intestinal glucose transport, and increases intestinal glucose utilization, all of which contribute to the blood glucose-lowering effects of metformin in diabetics. Increased intestinal glucose utilization is thought to contribute to metformin-induced intestinal lactic acidosis. Studies show that the highest accumulation of metformin occurs in the intestine following oral administration, which raises the question whether high metformin intestinal concentrations modulate cell function. Since intestinal glucose absorption occurs from the apical (AP) and basolateral (BL) membranes, it warrants investigating whether high metformin concentrations affect intestinal glucose absorption and glucose transporter (GLUT) translocation to the membranes of intestinal cells. There is little information about how metformin mediates GLUT transporters, although some evidence shows that metformin promotes translocation of GLUT transporters to the AP membrane. This study aims at elucidating the effect of metformin on glucose uptake and transport as a result of the GLUT transporters being translocated to AP and BL membranes of Caco-2 cell monolayers, a well-established model of human intestinal epithelia. Real-time polymerase chain reaction to determine relative expression of candidate glucose transporters GLUT1-3 in Caco-2 cells, and time- and concentration-dependent transport and uptake studies of the non-metabolizable radiolabeled glucose surrogate 2-deoxy-D-glucose (2DG) will provide information on the effect of metformin on intestinal glucose uptake and transport and contribute to knowledge about the risk of developing lactic acidosis.