Abstract
Glucagon-like peptide-1 (GLP-1) signaling modulates sweet-taste sensitivity in the mouse. Because circumvallate papillae (CVPs) express both GLP-1 and its receptor, a local regulation has been suggested. However, whether dietary lipids are involved in this regulation, as shown in the gut, is unknown. By using a combination of biochemical, immunohistochemical, and behavioral approaches, the present data i) confirm the role of GLP-1 signaling in the attraction for sucrose, ii) demonstrate that minute quantities of long-chain FAs (LCFAs) reinforce the attraction for sucrose in a GLP-1 receptor-dependent manner, iii) suggest an involvement of the LCFA receptor GPR120 expressed in taste buds in this system, and iv) support the existence of a regulation by GLP-1 of the lipid sensing mediated by lingual CD36. Therefore, oro-sensory detection of LCFAs may affect sweet and fatty taste responsiveness by controlling the secretion of lingual GLP-1. This regulatory loop, probably triggered by the LCFA-GPR120 interaction, might contribute to the high palatability of foods rich both in fat and sugar.
Highlights
Glucagon-like peptide-1 (GLP-1) signaling modulates sweet-taste sensitivity in the mouse
Addition of a small quantity of acid (OLA) or ␣-linolenic acid (ALA) or oleic acid (OLA) reinforced the avidity for the sucrose solution in wildtype mice, but was without effect in Glp1r-null mice (Fig. 1C), suggesting that long-chain FA (LCFA) may modulate sweet-taste sensitivity via the glucagon-like peptide-1 (GLP-1) signaling pathway
This behavior is independent of any change in relative expression of genes encoding for the gustatory lipid sensors GPR120 and CD36 in Glp1r-null mice (Fig. 2B, C)
Summary
Glucagon-like peptide-1 (GLP-1) signaling modulates sweet-taste sensitivity in the mouse. Two unrelated members of the G protein-coupled receptor family, the free fatty acid receptor 1 (FFAR1, termed GPR40) and GPR120, have been recently identified as playing a role in the spontaneous preference for fat in the mouse [11] Such a function is probably indirect for FFAR1, inasmuch as it is not found in taste buds in rat [12] and human [13] and is not systematically detected in circumvallate papillae (CVPs) in the mouse [8, 11], in contrast to GPR120. The fact that CD36 expression is subjected to a short-term lipid-mediated downregulation in mouse taste buds during food intake, whereas GPR120 gene expression remains unchanged [8], is consistent with distinct functions
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