The Role of GPR84 in Medium-chain Saturated Fatty Acid Taste Transduction

Abstract

It has been almost twenty years since investigators started to study the gustatory recognition of fatty acids, and in the interim most of the studies in this area have focused on the long-chain unsaturated fatty acids. However, medium-chain saturated fatty acids (MCFA) are also an important form of dietary fatty acids, and there is limited knowledge concerning the gustatory responsiveness to and possible transduction mechanisms of MCFAs in taste cells. In this study, I showed that MCFAs are effective taste stimuli at both the cellular and behavioral levels. To elucidate the mechanisms of gustatory recognition of MCFAs in mice, antagonists of several important players that might be involved in this pathway were used in electrophysiological experiments. Capric acid-induced currents were significantly inhibited by GDP-s-S and the inhibitors of protein kinase A (PKA) and protein kinase C (PKC), which suggested that the currents were activated downstream of G-protein, PKA and PKC activation. However, these currents were not affected by the phospholipase C (PLC) and phosphodiesterase (PDE) inhibitors, suggesting they were not involved in the MCFA taste transduction pathway. Further, loss of transient receptor potential channel type M5 (TRPM5) did not affect either the lauric acid-induced intracellular Ca2+ change or taste sensitivity to lauric acid, indicating that MCFA transduction in mouse taste cells is TRPM5-independent. My results indicated that MCFAs 52 are sapid compounds that work through a pathway that is independent of the welldocumented pathway for long-chain unsaturated fatty acids (Liu et al., 2011) and suggested increasing complexity to mechanisms underlying the ‘taste of fat’.