The sense of taste informs the body about the quality of ingested foods. Tastant-mediated signals are generated by a rise in free intracellular calcium levels ([Ca(2+)]i) in the taste bud cells and then are transferred to the gustatory area of brain via connections between the gustatory nerves (chorda tympani and glossopharyngeal nerves) and the nucleus of solitary tract in the brain stem. We have recently shown that lingual CD36 contributes to fat preference and early digestive secretions in the mouse. We show here that 1) the induction of an increase in [Ca(2+)]i by linoleic acid is CD36-dependent in taste receptor cells, 2) the spontaneous preference for or conversely conditioned aversion to linoleic acid requires intact gustatory nerves, and 3) the activation of gustatory neurons in the nucleus of the solitary tract elicited by a linoleic acid deposition on the tongue in wild-type mice cannot be reproduced in CD36-null animals. We conclude that the CD36-mediated perception of long-chain fatty acids involves the gustatory pathway, suggesting that the mouse may have a "taste" for fatty foods. This system would constitute a potential physiological advantage under conditions of food scarcity by leading the mouse to select and absorb fatty foods. However, it might also lead to a risk of obesity and associated diseases in a context of constantly abundant food.

We have recently demonstrated that the cells expressing CD36, localized apically on the taste buds of mouse lingual circumvallate papillae, act as gustatory cells. In the present study we isolated these CD36-positive cells from mouse circumvallate papillae and investigated intracellular signaling events, triggered by a long-chain polyunsaturated fatty acid, i.e. linoleic acid (LA). LA induced increases in free intracellular calcium concentrations, [Ca 2؉ ] i , by recruiting calcium from endoplasmic reticulum pool via inositol 1,4,5-triphosphate production followed by calcium influx via opening of store-operated calcium (SOC) channels. LA also induced phosphorylation of Srcprotein-tyrosine kinases (Src-PTKs), particularly of The tongue contains primarily four types of papillae. Filiforms are involved in the somesthesic perception of foods, whereas fungiforms, foliates, and circumvallates, which contain taste buds, are responsible for the chemosensory perception of basic taste modalities (sweet, bitter, salt, sour, umami (4) demonstrated that the addition of a lipase inhibitor diminished the spontaneous preference for triglycerides. These investigators proposed that the lingual lipase, present in the rodent saliva, might release free fatty acids that would be detected by gustatory cells. The immunolocalization of CD36 in the apical side of few TRC in circumvallate papillae (3) is especially adequate for this function since CD36 is known to exhibit a very high affinity for long-chain fatty acids (5). Consistent with this assumption, we have recently provided the first evidence that CD36-positive gustatory cells play a significant role in dietary lipid perception in the mouse (3). Indeed, the CD36 gene inactivation fully abolished the spontaneous preference for long-chain fatty acids observed in wild-type mice (3). It is noteworthy that this effect on feeding behavior is lipid-specific since sweet preference and bitter aversion are not affected in these transgenic mice (3).To further explore whether a sixth taste modality devoted to the "fat" functionally exists in rodents, the downstream signaling events triggered by the free fatty acid/CD36 interaction in gustatory cells must be studied. We have for the first time purified the CD36-positive gustatory cells from mouse CVP and demonstrated that linoleic acid induced increases in [Ca 2ϩ ] i in these cells via CD36 (6). In the present study we have extended these investigations to characterize the mechanisms of action of linoleic acid on calcium signaling/protein phosphorylation, leading to the release of neurotransmitters, which might be implicated in the activation of afferent nerve fibers.

NOUVELLE> L'obésité constitue indéniablement un des problèmes majeurs de santé publique de ce début du XXI e siècle. Sa préva-lence est en constante augmentation notamment chez les enfants. Ce constat n'est pas anodin car l'obésité est souvent associée à diverses pathologies graves (atteintes vasculaires, diabète de type 2, hypertension, cancer). L'opulence alimentaire, en nous permettant de satisfaire nos appétits spécifiques, contribue à ce phénomène. C'est ainsi que dans le régime occidental, les lipides alimentaires représentent près de 40 % des apports caloriques journaliers alors que les recommandations nutritionnelles sont inférieures de 5 à 10 %. L'origine de cette attirance pour les corps gras, encore mal connue, est également observée chez la souris. Dans cette espèce, on a longtemps pensé que la perception oro-sensorielle des lipides alimentaires dépendait uniquement de leurs propriétés olfactives et texturales. Cette vision quelque peu restrictive a récemment été battue en brè-che par une série d'expériences montrant que la gustation joue également un rôle important dans la préférence spontanée pour les corps gras. CD36 récepteur des acides gras à longue chaîneLe goût informe le système nerveux central sur la qualité des aliments ingérés conduisant ainsi à des comportements stéréotypés (attraction ou rejet) [1]. La perception des saveurs s'effectue par le biais de cellules réceptrices spécialisées (taste receptor cells, TRC) localisées dans les bourgeons du goût des papilles gustatives présentes essentiellement dans l'épithélium lingual. Nous avons récemment montré que la protéine CD36, connue pour lier les acides gras à longue chaîne (AGLC, nombre de carbones ≥ 16) avec une très haute affinité, est abondamment exprimée au niveau de certaines TRC chez la souris [2,9]. Cette glycoprotéine transmembranaire s'est avéré être impliquée dans la perception des lipides. En effet, l'invalidation du gène codant pour le CD36 diminue de façon drastique la préférence spontanée