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Enterally administered glucose modifies gut sensation, diminishes hunger, and slows gastric emptying by suppressing antral motility and stimulating pyloric pressures. We aimed to clarify the mechanism of small intestinal glucose sensing.We studied eight healthy males twice, in random order. An antroduodenal manometry catheter was positioned with a sleeve sensor across the pylorus. Benzocaine, or vehicle alone, was given into the proximal duodenum as a bolus, followed by continuous infusion for 105 min (T=−15 to 90 min). Glucose was also infused into the proximal duodenum at 3 kcal/min for 90 min (T=0–90 min). Sensations of hunger, bloating, and nausea were assessed with visual analog questionnaires, blood was sampled at intervals, and energy intake at a buffet meal (T=90–120 min) was measured.Perceptions of bloating and nausea were markedly less with benzocaine when compared with vehicle (P<0.05 for each), with no difference in hunger, or energy intake. In contrast, the suppression of antral waves and stimulation of phasic and tonic pyloric pressures, duodenal waves, and propagated duodenal wave sequences by intraduodenal glucose infusion did not differ between the 2 days. No difference in blood glucose, plasma insulin, or plasma glucagon-like peptide 1 between benzocaine and control was observed, whereas glucose-dependent insulinotropic polypeptide and cholecystokinin concentrations were slightly higher with benzocaine (P<0.05 for both).Mucosal anesthesia ameliorates unpleasant sensations induced by enteral glucose, but does not inhibit the release of gut peptides that feed back on appetite and gastroduodenal motility.