Exogenous oral application of PYY and exendin-4 impacts upon taste-related behavior and taste perception in wild-type mice.

Several gut peptides have been implicated in feeding and body mass accumulation. Glucagon-like peptide 1 (GLP-1) and peptide tyrosine-tyrosine (PYY) have been shown to mediate satiety and reduce food intake. While systemic administration of such peptides has been explored as a therapy for metabolic disease, the effects of these hormones on taste signaling should also be considered given the importance of taste to feeding decisions and considering the fact that components of these signaling systems are expressed in cells of the peripheral gustatory system. We previously demonstrated that genetic disruption of PYY signaling in mice can impact on taste responsiveness and feeding and that viral expression of PYY in the salivary glands of PYY knockout mice can rescue responsiveness. The present work uses adeno-associated virus-mediated salivary gland treatment with both GLP-1 receptor agonist exendin-4 and/or PYY encoding vectors to explore the effect of stimulating these orally present signaling systems on taste-related behavioral responsiveness in male wild-type mice with intact peptide signaling systems. Results showed a significant effect of salivary gland treatment on responsiveness to multiple taste qualities. Data gathered from taste bud cells in vitro suggest that these peptides directly influence the responsiveness of these primary sensory cells. Collectively, these findings show that taste perception can be modulated by the exogenous application of satiety peptides in wild-type mice and suggest that the taste bud is a promising substrate for food intake modulation.