Inhibition of gastric emptying by intestinal hexoses is dependent on absorption via sodium-glucose co-transporter (SGLT1)

Nutrients in the intestine initiate feedback inhibition of gastric emptying. The mechanism by which "sensors" in the intestine detect nutrients is unclear; carbohydrate-induced feedback inhibition is dependent on an intact extrinsic sensory innervation. The aim of this study was to determine (1) whether absorption via SGLT1 is required and (2) whether the hexose has to exit epithelial cells to initiate neurally-dependent feedback inhibition. Methods: Gastric emptying of liquids was measured in awake rats (n=12) fitted with gastric and duodenal fistulas. Glucose or mannitol (0.33, 0.66 or 1M), 3-O-methyl glucose (3OM), -methyl glucose (AMG) or 2-deoxyglucose (2DG) (0.33 M) were perfused into the duodenum and gastric emptying was measured over 10 min. Results: Perfusion of the duodenum with glucose inhibited gastric emptying from 72±2% to 47±5% (P<0.01). 3OM and AMG were not significantly different from glucose and inhibited gastric emptying to 52±8% and 55±7%, respectively. Mannitol and 2DG had no significant effect on gastric emptying. Conclusions:. The effect of carbohydrates on gastric emptying is independent of osmolarity but is dependent on absorption by the SGLT1. The effectiveness of AMG, which is a substrate for the SGLT1 on the apical surface of intestinal epithelial cells, but is not a substrate for the basolateral glucose transporter, suggests that the signal to intestinal "sensors" is generated within epithelial cells.