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      Modulation of taste sensitivity by GLP-1 signaling.

      Journal of Neurochemistry
      Animals, Citric Acid, pharmacology, Epithelial Cells, cytology, drug effects, metabolism, Glucagon-Like Peptide 1, Macaca, Mice, Mice, Knockout, Rats, Rats, Sprague-Dawley, Receptors, Glucagon, genetics, Sensory Receptor Cells, Sensory Thresholds, physiology, Signal Transduction, Sweetening Agents, Taste, Taste Buds, Visceral Afferents

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          Abstract

          In many sensory systems, stimulus sensitivity is dynamically modulated through mechanisms of peripheral adaptation, efferent input, or hormonal action. In this way, responses to sensory stimuli can be optimized in the context of both the environment and the physiological state of the animal. Although the gustatory system critically influences food preference, food intake and metabolic homeostasis, the mechanisms for modulating taste sensitivity are poorly understood. In this study, we report that glucagon-like peptide-1 (GLP-1) signaling in taste buds modulates taste sensitivity in behaving mice. We find that GLP-1 is produced in two distinct subsets of mammalian taste cells, while the GLP-1 receptor is expressed on adjacent intragemmal afferent nerve fibers. GLP-1 receptor knockout mice show dramatically reduced taste responses to sweeteners in behavioral assays, indicating that GLP-1 signaling normally acts to maintain or enhance sweet taste sensitivity. A modest increase in citric acid taste sensitivity in these knockout mice suggests GLP-1 signaling may modulate sour taste, as well. Together, these findings suggest a novel paracrine mechanism for the regulation of taste function.

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