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The intestinal absorption of glucose is mainly mediated by Sodium/glucose cotransporter 1 (SGLT1) at low luminal glucose concentrations, with Glucose transporter type 2 (GLUT2) participating in both facilitated diffusion across the basolateral membrane and, at higher glucose concentrations, also the apical membrane of enterocytes[1][2]. SGLT1 is the principal active transporter responsible for the uptake of dietary glucose from the small intestinal lumen into enterocytes, utilizing the sodium gradient as its energy source. At high carbohydrate loads, GLUT2 can be translocated to the apical (brush border) membrane to allow rapid facilitated diffusion of glucose[1][2][4]. Both transporters are implicated in glycemic control and are upregulated in diabetes, making them important therapeutic targets. Inhibitors of SGLT1 are used or under development for the treatment of diabetes mellitus, aiming to reduce intestinal glucose uptake and subsequent hyperglycemia without significant gastrointestinal side effects[1][2].
Inhibition of intestinal glucose absorption by blocking SGLT1. Delay or reduction of postprandial glucose rise. Potential modulation of incretin hormone secretion.
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