Suppression of sweet sensing with glucose, but not aspartame, delays gastric emptying and glycemic response.

Previously, we reported that oral stimulation with Gymnema sylvestre (GS), a plant that selectively suppresses sweet taste sensation in humans, delayed gastric emptying and glycemic response during and after oral glucose ingestion. It is unclear whether these responses are triggered by sweet taste sensing per se. We tested the hypothesis that the effects of sweet taste sensing involving a low-energy sweetener, aspartame, alters gastric emptying, blood glucose, and plasma insulin responses during and after the prandial phase. Nine participants rinsed their mouths with either 25 mL of water (control) or a 2.5% GS solution, and then ingested 200 g (50 g × four times) of either 0.09% aspartame or 15% glucose solution containing 100 mg of C-sodium acetate. Gastric emptying was measured with a C breath test. Blood glucose and plasma insulin were measured at baseline as well as during and after ingestion of the sweet solutions. Decreased subjective sweet taste intensity was observed in the GS group for both the aspartame and glucose trials. In the aspartame trial, no measurements showed significant differences between either group. In the glucose trial, gastric emptying was delayed in the GS group compared to controls. In the initial phase, both during and after glucose ingestion in the glucose trial, blood glucose and plasma insulin responses were lower in the GS group than the controls. The presence or absence of sweet taste-sensing involving glucose had a significant effect on gastric emptying and glycemic metabolism, both during and after the prandial phase, as opposed to the effects involving aspartame.