Presentation Details
| Nutritional Reprogramming of Oral Glucosensing Sandrine Chometton1, Lindsey A.Schier2. 1Université Bourgogne Europe, Institut Agro, CNRS, INRAE, UMR CSGA, Dijon, France.2Department of Biological Sciences, University of Southern California, Los Angeles, CA, USA |
Abstract
Glucose is an essential source of energy for all living organisms. Because this nutrient is mainly provided by the diet, it is necessary for the body to rapidly detect and motivate the ingestion of glucose-containing substances. The oral taste system is critical for recognizing nutrients in the environment and initiating ingestion. Chemically- and metabolically-diverse compounds including simple sugars, like glucose, low-calorie sweeteners, and D-amino acids engage a common “sweet taste” receptor (T1R2+T1R3), yet rodents will preferentially consume glucose over these other substrates over the long term. Our recent work demonstrates that experience with the post-ingestive effects of two metabolically distinct sugars, glucose and fructose, enables animals to subsequently discriminate these two initially similar-tasting compounds based on orosensory information, and generates a preference for glucose over fructose. This result has also been observed in mice lacking the canonical sweet taste receptor, showing that a T1R-independent pathway is involved. In this talk, I will present recent evidence we uncovered for how the post-ingestive effects of sugar reprogram metabolism-dependent and -independent glucosensing pathways in the taste bud cells, and amplify the responsiveness of taste neurons in the rostral nucleus of the solitary tract to oral glucose, in a T1R-independent fashion. Overall, these findings expand our understanding of orosensory mechanisms underlying glucose appetition.
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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.