Taste of glucose elicits cephalic-phase insulin release in mice

• Published in: Physiology & behavior Vol. 192; pp. 200 - 205
• Main Authors: Glendinning, John I., Lubitz, Gabrielle S., Shelling, Sarah
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.08.2018
• Subjects: Cephalic-phase insulin release; Glucose; KATP channel; Mice; Sugar; Taste; Taste; Mice; Glucose; KATP channel; Cephalic-phase insulin release; Sugar; K(ATP) channel
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/j.physbeh.2018.04.002

We reported previously that when C57BL/6 (B6) mice ingest glucose, plasma insulin levels rise above baseline before blood glucose levels do so. This observation led us to speculate that the taste of glucose elicits cephalic-phase insulin release (CPIR) in mice. Here, we examined the specific contributions of taste and glucose to CPIR. In Experiment 1, we bypassed the mouth and delivered glucose directly to the stomach. We found that plasma insulin levels did not rise above baseline until after blood glucose levels did so. This revealed that taste stimulation is necessary for rapid insulin release (i.e., CPIR) in mice. In Experiment 2, we examined the observation that sucrose, maltose and Polycose (a maltodextrin) all elicit CPIR. We proposed in a prior study that these carbohydrates did not directly elicit CPIR; instead, they were digested by oral amylases and alpha-glucosidases, and that it was the enzymatically liberated glucose that elicited CPIR. In support of this possibility, we reported that acarbose (an alpha-glucosidase inhibitor) prevented sucrose, maltose and Polycose from eliciting CPIR. Here, we sought to confirm that glucose alone could elicit CPIR in the presence of acarbose. Indeed, we found that glucose alone and glucose+acarbose each elicited equally robust CPIR. Taken together, these results provide further support for the hypothesis that mice possess a glucose-specific taste transduction pathway that triggers rapid insulin release.