An animal's ability to detect sweet-tasting compounds like glucose is critical for its survival, as sweet taste signals a nutrient-rich energy source. Likewise, sweet is the most universally palatable and reinforcing of all taste qualities, and highly impacts feeding behaviors: the more palatable a compound is, the more it is consumed. This role for taste in feeding is mirrored in the gut, where glucose-sensitive cells express the same molecular machinery required for sweet taste detection. Taste receptors in the gut detect sugars and other sweeteners and, via secretion of gut hormones, facilitate their absorption and initiate neural feedback onto feeding circuits in the brain. In this way, the sense of taste is extended to the gut, where it regulates ingestive behaviors and glucose homeostasis. Glucose homeostasis is regulated in part by a number of peptide hormones secreted in the gut, pancreas, and other digestive organs. For some of these hormones, links to the taste system are evident. For example, glucagon-like peptide 1 (GLP-1), a regulator of insulin biosynthesis and release, is secreted by gut enteroendocrine L cells in response to activation of sweet taste receptors on their surface. Our group has reported that GLP-1 and its receptor are also expressed in taste buds, where GLP-1 appears to modulate sweet taste sensitivity through local paracrine signaling. GLP-1 is processed from proglucagon, the same prohormone that produces glucagon. Glucagon is a major counter-regulatory hormone that works with insulin to maintain glucose homeostasis in the bloodstream. I have found that glucagon and its receptor are also expressed in taste cells of the tongue, though the role of glucagon signaling in taste remains unclear. In two specific aims, I will test the hypothesis that glucagon modulates sweet taste sensitivity through local signaling in the taste bud. I predict that (1) components of glucagon signaling are present in taste buds;and (2) that these glucagon signaling modulates taste behaviors. The ability of glucagon and other hormones (e.g., GLP-1) to modulate responsiveness to sweet-tasting stimuli suggests a mechanism by which an animal's metabolic state can impact sensory functions and ingestive behaviors. Furthermore, it suggests that aberrant hormonal signaling in conditions such as hypoglycemia, obesity and diabetes may yield abnormal reactivity to sweet tasting compounds, which could, in turn, lead to unhealthy eating behaviors.

National Institute of Health (NIH)
National Institute on Deafness and Other Communication Disorders (NIDCD)
Predoctoral Individual National Research Service Award (F31)
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Communication Disorders Review Committee (CDRC)
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Cyr, Janet
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University of Maryland Baltimore
Anatomy/Cell Biology
Schools of Medicine
United States
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Glendinning, John I; Elson, Amanda E T; Kalik, Salina et al. (2015) Taste responsiveness to sweeteners is resistant to elevations in plasma leptin. Chem Senses 40:223-31
Elson, Amanda E T; Dotson, Cedrick D; Egan, Josephine M et al. (2010) Glucagon signaling modulates sweet taste responsiveness. FASEB J 24:3960-9