CD36 and two G-protein coupled receptors (GPCR), i.e., GPR120 and GPR40, have been implicated in the gustatory perception of dietary fats in rodents. These glycoproteins are coupled to increases in free intracellular Ca²⁺ concentrations, [Ca²⁺](i), during their activation by dietary long-chain fatty acids (LCFA). The transient receptor potential type M5 (TRPM5) channel, activated by [Ca²⁺](i), participates in downstream signaling in taste bud cells (TBC). The mice, knocked-out for expression of CD36, GPR120, GPR40 or TRPM5 have a reduced spontaneous preference for fat. The delayed rectifying K⁺ (DRK) channels believed to lie downstream of these receptors are also important players in fat taste transduction. The trigeminal neurons by triggering increases in [Ca²⁺](i) may influence the taste signal to afferent nerve fibers. Why are there so many taste receptor candidates for one taste modality? We discuss the recent advances on the role of CD36, GPR120, GPR40, TRPM5 and DRK channels, in signal transduction in TBC. We shed light on their cross-talk and delineate their roles in obesity as a better understanding of the molecular mechanisms behind their regulation could eventually lead to new strategies to fight against this condition.
Keywords: Calcium signaling; DRK channels; Fat taste; Obesity; Signal transduction; TRPM channels.
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