Presentation Details
| Adiponectin signaling modulates fat taste responsiveness and sensitivity in mice Fangjun Lin1, Timothy A.Gilbertson2. 1Burnett School of Biomedical Sciences, University of Ceentral Florida, Orlando, FL, USA.2Department of Internal Medicine, University of Central Florida, Orlando, FL, USA |
Abstract
Adiponectin is a fat tissue-derived hormone with insulin-sensitizing and anti-inflammatory functions. Adiponectin receptors are highly expressed in taste buds, suggesting a potential role of adiponectin signaling in the modulation of taste function. Previously, we showed that the adiponectin receptor agonist, AdipoRon, acts to enhance calcium responses to fatty acids in human taste cells by increasing the translocation of CD36 to the cell surface (Lin et al. Int J Mol Sci 24:5801, 2023). Using calcium imaging, we found that adiponectin and AdipoRon enhances cellular responses to fatty acids in isolated taste bud cells from male and female wild-type (WT) mice, but not AdipoR1 knockout (KO) mice. Two-bottle preference and conditioned taste aversion behavioral assays in AdipoR1 KO mice indicated a critical, sex-dependent role for adiponectin signaling in the modulation of taste responsiveness. Female AdipoR1 KO mice showed a diminished preference and reduced taste sensitivity for linoleic acid compared to WT controls, while no such differences were found in male AdipoR1 KO and WT mice. No significant differences were seen in their preference for sweet, bitter, umami, and sour stimuli in either sex. Moreover, loss of AdipoR1 did not appear to significantly inhibit the strong preference for or intake of either Intralipid or a high fat diet. Together, these data indicate that adiponectin acts via AdipoR1 in mouse taste bud cells to enhance their responses to fatty acids and adiponectin signaling may play a key role in the recognition of fatty acids, however, such taste modulation by AdipoR1 signaling alone does not appear to effect significantly dietary fat intake. Supported by NIH DC013318 (tag).
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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.