Hormonal modulation of taste

Abstract

The gustatory system provides critical information about the quality and nutritional value of food before it is ingested. Of the known taste qualities, sweet is the most palatable, and often signals foods that are calorically-dense. Thus, an animal's ability to detect sweet foods is essential for its survival. Balance, however, is paramount, and numerous hormones work to modulate food intake in the context of nutritional needs and metabolic status. Many of these hormones also modulate taste responsiveness to sweet stimuli. For example, glucagon-like peptide-1, which prepares the body to accept incoming nutrients, is also produced in taste buds. There, it appears to either enhance or maintain taste responsiveness to sweet stimuli through local actions on their cognate receptors. In addition, leptin, which signals to the rest of the body the amount of energy stored as fat, also acts on taste cells through its receptor, and appears to decrease responses to sweet. The work in this dissertation seeks to identify how another hormone, glucagon, a promoter of glucose homeostasis, might modulate sweet taste. The first set of studies characterizes the immunohistochemical expression patterns of glucagon in taste cells, and its role in taste behaviors. I show that glucagon and its receptor are expressed on a subset of taste cells that are likely sweet-sensitive, and that glucagon works to maintain or enhance responsiveness to sweet, but not other taste qualities. The second set of studies seeks to determine if glucagon can work in concert with leptin to modulate behavioral responsiveness to sweet. Here, I show that leptin's actions on sweet taste are actually dependent on the sucrose concentration used: leptin decreases responsiveness to high concentrations, but enhances or maintains responsiveness to low concentrations. Furthermore, combining leptin and glucagon manipulations did not result in additional taste suppression in either sucrose range. However, leptin treatment "rescued" the suppressive effects of disrupted glucagon signaling in the low sucrose range. I also show immunohistochemical evidence that the leptin receptor and glucagon are expressed on the same taste cells. In aggregate, these data suggest that glucagon and leptin modulate sweet taste responsiveness in a context-dependent manner.