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Publication : Greater reductions in fat preferences in CALHM1 than CD36 knockout mice.

First Author  Sclafani A Year  2018
Journal  Am J Physiol Regul Integr Comp Physiol Volume  315
Issue  3 Pages  R576-R585
PubMed ID  29768036 Mgi Jnum  J:264580
Mgi Id  MGI:6196414 Doi  10.1152/ajpregu.00015.2018
Citation  Sclafani A, et al. (2018) Greater reductions in fat preferences in CALHM1 than CD36 knockout mice. Am J Physiol Regul Integr Comp Physiol 315(3):R576-R585
abstractText  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. Naive 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.
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