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Publication : The oral lipid sensor GPR120 is not indispensable for the orosensory detection of dietary lipids in mice.

First Author  Ancel D Year  2015
Journal  J Lipid Res Volume  56
Issue  2 Pages  369-78
PubMed ID  25489006 Mgi Jnum  J:219835
Mgi Id  MGI:5629803 Doi  10.1194/jlr.M055202
Citation  Ancel D, et al. (2015) The oral lipid sensor GPR120 is not indispensable for the orosensory detection of dietary lipids in mice. J Lipid Res 56(2):369-78
abstractText  Implication of the long-chain fatty acid (LCFA) receptor GPR120, also termed free fatty acid receptor 4, in the taste-guided preference for lipids is a matter of debate. To further unravel the role of GPR120 in the "taste of fat", the present study was conducted on GPR120-null mice and their wild-type littermates. Using a combination of morphological [i.e., immunohistochemical staining of circumvallate papillae (CVP)], behavioral (i.e., two-bottle preference tests, licking tests and conditioned taste aversion) and functional studies [i.e., calcium imaging in freshly isolated taste bud cells (TBCs)], we show that absence of GPR120 in the oral cavity was not associated with changes in i) gross anatomy of CVP, ii) LCFA-mediated increases in intracellular calcium levels ([Ca(2+)]i), iii) preference for oily and LCFA solutions and iv) conditioned avoidance of LCFA solutions. In contrast, the rise in [Ca(2+)]i triggered by grifolic acid, a specific GPR120 agonist, was dramatically curtailed when the GPR120 gene was lacking. Taken together, these data demonstrate that activation of lingual GPR120 and preference for fat are not connected, suggesting that GPR120 expressed in TBCs is not absolutely required for oral fat detection in mice.
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