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Intestinal glucose absorption pathways consist mainly of two essential membrane transporters: the sodium-dependent glucose cotransporter 1 (SGLT1), which actively transports glucose across the apical (luminal) membrane of intestinal enterocytes in conjunction with sodium, and the facilitated glucose transporter type 2 (GLUT2), which conducts high-capacity, passive facilitated diffusion across the basolateral membrane into the bloodstream. At high luminal glucose concentrations, GLUT2 can also be transiently inserted in the apical membrane, augmenting absorption[1][2][4][5][6]. These pathways are regulated by dietary intake, gut hormones, and cellular signaling (e.g., PKC, MAPK pathways)[2]. Disruption of these pathways is implicated in diseases such as diabetes and genetic malabsorption syndromes, making SGLT1 and GLUT2 important therapeutic targets for controlling postprandial glucose levels and metabolic disease risk[1][5][6].
Inhibition of sodium-glucose cotransport (reducing intestinal glucose absorption and postprandial glucose spikes); Inhibition of GLUT2-mediated facilitated diffusion (experimental, less clinically targeted)
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