SPLTRAK Abstract Submission
Ghrelin Alters Fatty Acid Signaling in Taste Cells
Ashley N. Calder1,2, Naima S. Dahir1,2, Tian Yu3, Timothy A. Gilbertson2
1Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, United States
2Department of Internal Medicine, College of Medicine, University of Central Florida, Orlando, FL, United States
3Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, United States

Ghrelin has long been implicated in energy homeostasis and is thought to regulate caloric consumption. Secreted by gastric emptying, circulating ghrelin has been shown to work in diverse physiological pathways including caloric intake, glucose regulation, and lipid storage. Previous data have shown that ghrelin and its receptor are located in the taste system. Mice lacking ghrelin have a decreased caloric intake and altered lipid preferences (Cai et al., PLoS One 8(10), 2013). To date, limited research has explored the role of ghrelin in fat taste. Previous work in our lab demonstrated high levels of co-localization between growth-hormone secratogue receptor (GHSR), a ghrelin receptor, and markers for Type II cells, the main cells responsible for fat taste transduction. The current study is aimed at evaluating the functional role of ghrelin in fat taste using ghrelin-null mice and WT mice. To date, we found that taste cells from ghrelin-null mice have functionally altered taste responses to fatty acids (FA) as illustrated by calcium imaging than WT mice. GPR120 and CD36, key components in the initial receptive events in the FA taste transduction pathway, have been shown to be downregulated in mice lacking the ghrelin hormone. To corroborate this, we plan to compare expression of GPR120, CD36, and other FA signaling proteins such as Kv1.5 and TRPM5 in ghrelin-null and WT mice. Additionally, we hypothesize that taste cells primed with ghrelin in combination with fatty acids will show a remarkable change in cellular activity compared to their WT counterparts. Given that obesity is fueled, in part, by overconsumption in response to altered fat taste, our data suggest circulating ghrelin may play a role in these changes to taste cell responsiveness. Supported by NIH DC013194 and DC013318 (tag).