Oral glucose sensing in cephalic phase insulin release

Oral stimulation with foods or food components elicits cephalic phase insulin release (CPIR), which limits postprandial hyperglycemia. Despite its physiological importance, the specific gustatory mechanisms that elicit CPIR have not been clearly defined. While most studies point to glucose and glucose-containing saccharides (e.g., sucrose, maltodextrins) as being the most consistent elicitors, it is not apparent whether this is due to the detection of glucose per se, or to the perceived taste cues associated with these stimuli (e.g., sweetness, starchiness). This study investigated potential sensory mechanisms involved with eliciting CPIR in humans, focusing on the role of oral glucose detection and associated taste. Four stimulus conditions possessing different carbohydrate and taste profiles were designed: 1) glucose alone; 2) glucose mixed with lactisole, a sweet taste inhibitor; 3) maltodextrin, which is digested to starchy- and sweet-tasting products during oral processing; and 4) maltodextrin mixed with lactisole and acarbose, an oral digestion inhibitor. Healthy adults (N = 22) attended four sessions where blood samples were drawn before and after oral stimulation with one of the target stimuli. Plasma c-peptide, insulin, and glucose concentrations were then analyzed. Whereas glucose alone elicited CPIR (one-sample t-test, p < 0.05), it did not stimulate the response in the presence of lactisole. Likewise, maltodextrin alone stimulated CPIR (p < 0.05), but maltodextrin with lactisole and acarbose did not. Together, these findings indicate that glucose is an effective CPIR stimulus, but that an associated taste sensation also serves as an important cue for triggering this response in humans.