Sodium-glucose cotransporter 1 (SGLT1)

"Glucose absorption in intestine" is not itself a molecular target but describes a physiological process primarily mediated by specific transporters. The key molecular target responsible for intestinal glucose absorption is Sodium-glucose cotransporter 1 (SGLT1). This transporter is located on the apical membrane of enterocytes lining the small intestine and mediates active uptake of dietary glucose from the lumen into cells using energy from sodium gradients[4][6]. After entry via SGLT1, glucose exits into circulation through basolateral facilitative transporters such as GLUT2[2][3]. SGLT1 also plays an essential role in glucose-induced incretin hormone secretion—notably GIP and GLP‑1—which are important for insulin release after meals[2]. Loss or inhibition of SGLT1 drastically reduces both intestinal glucose uptake and incretin responses[2][3]. While GLUT2 has been proposed to contribute to bulk facilitated diffusion under high luminal concentrations, evidence indicates that SGLT1 remains indispensable even at high loads, with GLUT2's main role being basolateral exit rather than apical entry under most physiological conditions[3][5]. The query refers to "Glucose absorption in intestine" as if it were a single molecule or receptor. In reality, this term describes a process involving multiple proteins—primarily Sodium-glucose cotransporter 1 (SGLT1) but also including others like GLUT2. For structured data purposes, it should be mapped specifically to "Sodium-glucose cotransporter 1," not left as an unstructured process name[4][6].

Other names

Sodium-glucose linked transporter 1SLC5A1sodium-dependent glucose cotransporter 1

Inhibitors block active sodium-coupled glucose uptake at the apical membrane, reducing postprandial blood glucose rise.