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. 2012 Jun 7;97(8):2597–2605. doi: 10.1210/jc.2012-1475

Fig. 1.

Fig. 1.

A model of intestinal glucose absorption in the fasting or low luminal carbohydrate state (A) or after a high-carbohydrate meal, with or without non-nutritive sweeteners (B). In the low luminal carbohydrate state, glucose is largely transported from the gut lumen into the enterocyte via SGLT-1. Glucose may pass in a bidirectional manner between the enterocyte and the bloodstream via GLUT2 located on the basolateral membrane, depending on the plasma glucose concentration and the metabolic needs of the enterocyte. In the presence of high luminal carbohydrate, glucose binds to sweet-taste receptors on enteroendocrine L cells, initiating a signal transduction cascade that results in GLP-1 and GLP-2 release. GLP-2 may cause up-regulation of SGLT-1 via enteric neurons. GLP-1 may act in a paracrine manner on nearby enterocytes to up-regulate apical GLUT2. Non-nutritive sweeteners can also bind to enteroendocrine sweet-taste receptors, causing GLP-1 release (in vitro) and increased intestinal glucose uptake (in rodents).