Several studies indicate an important role of gustation in intake and preference for dietary fat. The present study compared fat preference deficits produced by deletion of CD36, a putative fatty acid taste receptor, and CALHM1, an ion channel responsible for release of the ATP neurotransmitter used by taste cells. Naïve CD36 knockout (KO) mice displayed reduced preferences for soybean oil emulsions (Intralipid) at low concentrations (0.1–1%) compared with wild-type (WT) mice in 24 h/day two-bottle tests. CALHM1 KO mice displayed even greater Intralipid preference deficits compared with WT and CD36 KO mice. These findings indicate that there may be another taste receptor besides CD36 that contributes to fat detection and preference. After experience with concentrated fat (2.5–5%), CD36 KO and CALHM1 KO mice displayed normal preferences for 0.1–5% fat, although they still consumed less fat than WT mice. The experience-induced rescue of fat preferences in KO mice can be attributed to postoral fat conditioning. Short-term (3-min) two-bottle tests further documented the fat preference deficits in CALHM1 KO mice but also revealed residual preferences for concentrated fat (5–10%), which may be mediated by odor and/or texture cues.
Maltodextrin and Fat Preference Deficits in "Taste-Blind" P2X2/P2X3 Knockout Mice
