Fatty acid responses in taste cells from obesity-prone and -resistant rats.

One of the transduction mechanisms for the chemoreception of fat has been proposed to involve the inhibition of delayed rectifying potassium (DRK) channels by polyunsaturated free fatty acids (PUFAs). In the present study we have compared the responsiveness of fungiform taste receptor cells (TRCs) to fatty acids in obesity-prone (Osborne-Mendel; O-M) and obesity-resistant (S5B/Pl) rat strains using patch clamp recording. TRCs from S5B/Pl rats were markedly more responsive to PUFAs than those from O-M, yet with identical inhibition constants. Moreover, addition of PUFAs to subthreshold concentrations of saccharin enhanced preference for the mixture in two-bottle preference tests compared to the saccharin alone in S5B/Pl but not O-M rats. The correlation between electrophysiological and behavioral effects of PUFAs suggested that differences in fatty acid-sensitive DRK expression may underlie the phenotypic differences between S5B/Pl and O-M rats. Consistent with this hypothesis, O-M rats exhibit a greater DRK current density and express quantitatively more DRK channels as assayed using quantitative real-time PCR. No differences were found when comparing expression of fatty acid activated two pore domain potassium channels. We propose that the ratio of fatty acid-sensitive DRK channels to fatty acid-insensitive DRK channels may be important to contributing to overall peripheral fatty acid sensitivity and in that way influence the strength of the resulting chemosensory response to fat.