Presentation Details
| Evidence for a glucose-specific taste pathway that triggers insulin release in naïve B6 mice John I.Glendinning1, Natalie Ashkar1, Kiriaki Georgiou1, Ashley Guardado1, Julia Istefanos1, Nidhi Khanchumarti 1, Yixin Jia4, Janet Liu1, Kathryn Medler3, Laura Mittelman1, Sarah Nordlicht1, Clara Resnick1, Abigail Spingarn1, Anne-Marie Torregrossa2. 1Barnard College, Columbia University, New York, NY, USA.2University at Buffalo, Buffalo, NY, USA.3Virginia Tech, Blacksburg, VA, USA.4Monell Chemical Senses Center, Philadelphia, PA, USA |
Abstract
The cephalic-phase insulin response (CPIR) is elicited by food-related stimuli. It causes a rapid rise in plasma insulin, and promotes the disposal of glucose during and after meals. Here, we conducted 6 experiments to explore the mechanistic basis of a specific type of CPIR, which is elicited by the ingestion of solutions containing glucose or glucose-containing carbohydrates in sugar-naïve mice. First, we used IP3R3 receptor knock-out (KO) mice to determine whether this receptor—a critical component of the T1R2+R3 sweet taste pathway—is necessary for D-glucose to elicit a CPIR. We found that deletion of the IP3R3 receptor had no impact on the glucose-induced CPIR. Second, we asked whether D-glucose elicits a peripheral taste response in IP3R3 receptor KO mice. We observed a chorda tympani nerve response to lingual stimulation with D-glucose, but not sucrose, fructose or saccharin. Third, we determined whether flushing the mouth with D-glucose was sufficient to elicit a CPIR in B6 mice. We found that flushing with D-glucose but not fructose elicited a CPIR. Fourth, we asked whether stimulation of the T1R2+R3 taste pathway with saccharin enhanced the CPIR to D-glucose. We did not observe any enhancement. Fifth, we reasoned that if the CPIR is mediated by a glucose-specific taste pathway analogous to the one in pancreatic beta cells, then it should be triggered by ingestion of D-glucose but not L-glucose or isomaltulose. As predicted, D-glucose alone triggered a CPIR. Sixth, given that D-glucose evokes a salient odor in mice, we predicted that olfactory input may contribute to the glucose-induced CPIR. Olfactory impairment had no impact. These results provide multiple lines of support for the hypothesis that the glucose-induced CPIR is initiated by activation of a glucose-specific taste pathway.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
Content Locked. Log into a registered attendee account to access this presentation.