Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and 'exit' via the basolateral membrane proteins.

The classical pathway for this absorption across the intestinal membrane is mediated by a symporter, sodium-glucose linked transporter 1 (SGLT1). SGLT1 is present on the apical membrane of intestinal epithelial cells and couples the transport sodium ions and the monosaccharides l(glucose or galactose) into the cell.

The absorption of glucose in the small intestinal epithelium is electrogenic, depending on the membrane potential of the intestinal epithelial cells that regulate the activity of SGLT1. The maintenance of membrane potential depends on the activities of the channels and transporters. In the small intestine's epithelial cells, the potassium channels provide the driving force required for sodium-dependent uptake of glucose into the intestinal epithelial cells. The glucose uptake is further driven by the sodium transmembrane gradient and membrane potential maintained by the sodium-potassium pump. Thus, the sodium-potassium pump and potassium channel play a vital role in the glucose movement into the cell. The accumulated glucose is transported via GLUT2 transporter protein on the basolateral membrane.

Metabolic disorders like diabetes show increased expression of SGLT1, contributing to increased glucose absorption in the small intestine. Therefore, reducing the SGLT1-mediated transport of glucose appears to be one of the therapeutic targets for diabetes treatment.