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• W2150804024 abstract "A relationship between orosensory detection of dietary lipids, regulation of fat intake, and body mass index was recently suggested. However, involved mechanisms are poorly understood. Moreover, whether obesity can directly modulate preference for fatty foods remains unknown. To address this question, exploration of the oral lipid sensing system was undertaken in diet-induced obese (DIO) mice. By using a combination of biochemical, physiological, and behavioral approaches, we found that i) the attraction for lipids is decreased in obese mice, ii) this behavioral change has an orosensory origin, iii) it is reversed in calorie-restricted DIO mice, revealing an inverse correlation between fat preference and adipose tissue size, iv) obesity suppresses the lipid-mediated downregulation of the lipid-sensor CD36 in circumvallate papillae, usually found during the refeeding of lean mice, and v) the CD36-dependent signaling cascade controlling the intracellular calcium levels ([Ca2+]i) in taste bud cells is decreased in obese mice. Therefore, obesity alters the lipid-sensing system responsible for the oral perception of dietary lipids. This phenomenon seems to take place through a CD36-mediated mechanism, leading to changes in eating behavior. A relationship between orosensory detection of dietary lipids, regulation of fat intake, and body mass index was recently suggested. However, involved mechanisms are poorly understood. Moreover, whether obesity can directly modulate preference for fatty foods remains unknown. To address this question, exploration of the oral lipid sensing system was undertaken in diet-induced obese (DIO) mice. By using a combination of biochemical, physiological, and behavioral approaches, we found that i) the attraction for lipids is decreased in obese mice, ii) this behavioral change has an orosensory origin, iii) it is reversed in calorie-restricted DIO mice, revealing an inverse correlation between fat preference and adipose tissue size, iv) obesity suppresses the lipid-mediated downregulation of the lipid-sensor CD36 in circumvallate papillae, usually found during the refeeding of lean mice, and v) the CD36-dependent signaling cascade controlling the intracellular calcium levels ([Ca2+]i) in taste bud cells is decreased in obese mice. Therefore, obesity alters the lipid-sensing system responsible for the oral perception of dietary lipids. This phenomenon seems to take place through a CD36-mediated mechanism, leading to changes in eating behavior. Existence of an attraction for dietary lipids is observed in both rodents (1Tsuruta M. Kawada T. Fukuwatari T. Fushiki T. The orosensory recognition of long-chain fatty acids in rats.Physiol. Behav. 1999; 66: 285-288Crossref PubMed Scopus (105) Google Scholar, 2Takeda M. Imaizumi M. Fushiki T. Preference for vegetable oils in the two-bottle choice test in mice.Life Sci. 2000; 67: 197-204Crossref PubMed Scopus (65) Google Scholar–3Takeda M. Imaizumi M. Sawano S. Manabe Y. Fushiki T. Long-term optional ingestion of corn oil induces excessive caloric intake and obesity in mice.Nutrition. 2001; 17: 117-120Crossref PubMed Scopus (34) Google Scholar) and humans (4Drewnowski A. Greenwood M.R. Cream and sugar: human preferences for high-fat foods.Physiol. Behav. 1983; 30: 629-633Crossref PubMed Scopus (299) Google Scholar, 5Nysenbaum A.N. Smart J.L. Sucking behaviour and milk intake of neonates in relation to milk fat content.Early Hum. Dev. 1982; 6: 205-213Crossref PubMed Scopus (39) Google Scholar). Over the last decade, mechanisms leading to this stereotyped behavior have been actively studied, and compelling evidence supports the implication of a taste component in the detection of lipids [i.e., long-chain fatty acids (LCFAs)], in addition to textural, olfactory and postingestive cues. In mice, it was shown that i) gene invalidation of two unrelated LCFA receptors specifically expressed in taste buds (i.e., CD36 and GPR120) renders animals unable to properly detect lipids during behavioral tests (6Laugerette F. Passilly-Degrace P. Patris B. Niot I. Febbraio M. Montmayeur J.P. Besnard P. CD36 involvement in orosensory detection of dietary lipids, spontaneous fat preference, and digestive secretions.J. Clin. Invest. 2005; 115: 3177-3184Crossref PubMed Scopus (501) Google Scholar, 7Cartoni C. Yasumatsu K. Ohkuri T. Shigemura N. Yoshida R. Godinot N. le Coutre J. Ninomiya Y. Damak S. Taste preference for fatty acids is mediated by GPR40 and GPR120.J. Neurosci. 2010; 30: 8376-8382Crossref PubMed Scopus (312) Google Scholar), ii) LCFAs trigger a signaling cascade in freshly isolated CD36-positive taste bud cells leading to a rise in [Ca2+]i and to a neurotransmitter release (8El-Yassimi A. Hichami A. Besnard P. Khan N.A. Linoleic acid induces calcium signaling, Src kinase phosphorylation, and neurotransmitter release in mouse CD36-positive gustatory cells.J. Biol. Chem. 2008; 283: 12949-12959Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 9Dramane G. Abdoul-Azize S. Hichami A. Vogtle T. Akpona S. Chouabe C. Sadou H. Nieswandt B. Besnard P. Khan N.A. STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice.J. Clin. Invest. 2012; 122: 2267-2282Crossref PubMed Scopus (62) Google Scholar), and iii) the subsequent lipid signal uses peripheral and central nervous circuitry involved in gustation (7Cartoni C. Yasumatsu K. Ohkuri T. Shigemura N. Yoshida R. Godinot N. le Coutre J. Ninomiya Y. Damak S. Taste preference for fatty acids is mediated by GPR40 and GPR120.J. Neurosci. 2010; 30: 8376-8382Crossref PubMed Scopus (312) Google Scholar, 10Gaillard D. Laugerette F. Darcel N. El-Yassimi A. Passilly-Degrace P. Hichami A. Khan N.A. Montmayeur J.P. Besnard P. The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse.FASEB J. 2008; 22: 1458-1468Crossref PubMed Scopus (181) Google Scholar). Recent data have highlighted important differences between lingual CD36 and GPR120 suggesting distinct, but complementary, functions in mouse taste buds. In contrast to GPR120, expression of CD36 protein in circumvallate papillae (CVP) is lipid sensitive (11Martin C. Passilly-Degrace P. Gaillard D. Merlin J.F. Chevrot M. Besnard P. The lipid-sensor candidates CD36 and GPR120 are differentially regulated by dietary lipids in mouse taste buds: impact on spontaneous fat preference.PLoS ONE. 2011; 6: e24014Crossref PubMed Scopus (127) Google Scholar). Indeed, lingual CD36 protein levels displayed a rapid decrease in CVP when fasted mice were refed a diet containing lipids. It was suggested that the lipid-mediated downregulation of CD36 in taste bud cells might modulate the motivation for fat consumption during a meal, initially high and then gradually decreasing secondary to the food intake, a phenomenon reminiscent of sensory-specific satiety (12Rolls E.T. The neurophysiology of feeding.Int. J. Obes. 1984; 8 (Suppl.): 139-150PubMed Google Scholar). For GPR120, an implication in the glucagon-like peptide-1 (GLP-1) release by mouse CVP, producing a modulation of sweet and “fatty” taste sensitivity, was proposed (13Martin C. Passilly-Degrace P. Chevrot M. Ancel D. Sparks S.M. Drucker D.J. Besnard P. Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity.J. Lipid Res. 2012; 53: 2256-2265Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar). Psychophysical experiments demonstrate that humans are also able to detect very low concentrations of LCFA in oral cavity under conditions in which textural and olfactory cues are minimized (14Chalé-Rush A. Burgess J.R. Mattes R.D. Evidence for human orosensory (taste?) sensitivity to free fatty acids.Chem. Senses. 2007; 32: 423-431Crossref PubMed Scopus (177) Google Scholar). Recent data suggest an implication of lingual CD36 in this phenomenon. Indeed, obese patients with the common single nucleotide polymorphism A/A genotype at rs1761667, known to reduce the CD36 gene expression (15Love-Gregory L. Sherva R. Schappe T. Qi J.S. McCrea J. Klein S. Connelly M.A. Abumrad N.A. Common CD36 SNPs reduce protein expression and may contribute to a protective atherogenic profile.Hum. Mol. Genet. 2011; 20: 193-201Crossref PubMed Scopus (116) Google Scholar), displayed a higher detection threshold (i.e., low fat perception sensitivity) for lipids than G/G controls (16Pepino M.Y. Love-Gregory L. Klein S. Abumrad N.A. The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects.J. Lipid Res. 2012; 53: 561-566Abstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar) and showed a greater attraction for added fats and oils (17Keller K.L. Liang L.C. Sakimura J. May D. van Belle C. Breen C. Driggin E. Tepper B.J. Lanzano P.C. Deng L. et al.Common variants in the CD36 gene are associated with oral fat perception, fat preferences, and obesity in African Americans.Obesity (Silver Spring). 2012; 20: 1066-1073Crossref PubMed Scopus (138) Google Scholar). Therefore, genetic predispositions may affect the preference for fat, which might induce changes in eating behavior and obesity risk. Given the obesity epidemic, an important alternative issue is to determine whether obesity itself leads to changes in the orosensory perception of dietary fat. Interestingly, a relationship between orosensory sensitivity for lipids and body mass index has been recently reported in human (18Stewart J.E. Feinle-Bisset C. Golding M. Delahunty C. Clifton P.M. Keast R.S. Oral sensitivity to fatty acids, food consumption and BMI in human subjects.Br. J. Nutr. 2010; 104: 145-152Crossref PubMed Scopus (265) Google Scholar). Moreover, a comparison of obese and nonobese children and adolescents for the detection of sweet, umami, bitter, salty, and sour tastes demonstrates that obesity affects taste sensitivity. Indeed, obese subjects display a low ability to correctly identify the different taste modalities (19Overberg J. Hummel T. Krude H. Wiegand S. Differences in taste sensitivity between obese and non-obese children and adolescents.Arch. Dis. Child. 2012; 97: 1048-1052Crossref PubMed Scopus (117) Google Scholar). However, mechanisms involved in the modulation of taste sensitivity are poorly understood. To address this question, mice were subjected to nutritional challenges (obesogenic or calorie-restricted diets), and a combination of biochemical, physiological, and behavioral approaches was used to analyze the impact of obesity on fat preference. French guidelines for the use and the care of laboratory animals were followed, and experimental protocols were approved by the Animal Ethics Committee of Burgundy University. Six week-old C57Bl/6 mice were purchased from Charles River Laboratories, France. Animals were housed in filtered cages in a controlled environment (constant temperature and humidity, dark period from 7 PM to 7 AM). The mice had free access to tap water during the experiment. After a 1 week acclimatization period, the mice were fed ad libitum either a standard laboratory chow (4RF21, Mucedola, Italy; containing 3% fat, w/w) or two different obesogenic diets: a high-fat (HF) diet, rich in saturated FAs and a high-fat/high-sucrose (HFHS) diet (Table 1). Some diet-induced obese (DIO) mice fed the HF diet were calorie restricted (= 60% energy of ad libitum energy intake). Body mass and food consumption were recorded weekly. Body composition (fat mass, lean mass, and total body water) was measured by EchoMRI (Echo Medical Systems; Houston, TX).TABLE 1Diet compositionHFHFHSContents (% w/w)Control (4RF21 Mucedola)HF (4RF25 Mucedola + Palm oil)Control (Research Diet)HFHS (Research Diet)Proteins18.515.01926.2CarbohydratesStarch53.534.4163.1—Sucrose———26.1FatsSoya oil32.46.53.2Palm—31.8——Lard———31.7of whichSaturated FA0.516.7116.3Monounsaturated FA0.513.01.613.4Polyunsaturated FA1.34.53.95.1Energy(kcal/100g)315505.8386.9523.2 Open table in a new tab CVP from control and DIO mice were isolated according to the procedure described elsewhere (6Laugerette F. Passilly-Degrace P. Patris B. Niot I. Febbraio M. Montmayeur J.P. Besnard P. CD36 involvement in orosensory detection of dietary lipids, spontaneous fat preference, and digestive secretions.J. Clin. Invest. 2005; 115: 3177-3184Crossref PubMed Scopus (501) Google Scholar). Briefly, lingual epithelium was separated from connective tissue by enzymatic dissociation (elastase and dispase mixture, 2 mg/ml each in Tyrode buffer: 140 mM NaCl, 5 mM KCl, 10 mM HEPES, 1 mM CaCl2, 10 mM glucose, 1 mM MgCl2, 10 mM Na pyruvate, pH 7.4), and the papilla was dissected under a binocular microscope. CVP were either used immediately for the calcium imaging assays or snap-frozen in liquid nitrogen then stored at −80°C until CD36 determination by Western blotting. Plasma was obtained after centrifugation of blood (5,000 g for 10 min, 4°C). Plasma insulin levels were assayed by using a commercial ELISA kit (Mercodia, Sweden), and plasma glucose and triglyceride levels were determined with enzymatic reaction kits (Biomerieux, France). Two different tests, consisting of offering simultaneously a control and an experimental solution (two-bottle preference test) or successively in a randomized manner (licking test) were used. Mice were offered two bottles at the beginning of the dark period for 12 h. Control and experimental bottles contained 0.3% xanthan gum (w/v; Sigma-Aldrich) in water in order to emulsify the oil and to minimize textural cues between the two solutions. Animals were subjected to a choice between control or oily solution containing 0.02%, 0.2%, and 2.0% rapeseed oil (w/v), successively. To avoid the development of side preference, position of each bottle was inversed at each test. At the end of the test, the consumption of each solution was analyzed by weighing the bottles, and the percent of preference for the experimental solution was calculated (ratio consumption of the experimental solution upon total consumption). This test was performed to analyze the short-term (1–5 min) preference for an LCFA by using computer-controlled lickometers (Med Associates). Animals were successively subjected to the control or the experimental solution, and the number of licks given on each bottle by min was determined. Mice were food and water deprived 6 h before the test, which took place 6 h after the beginning of the dark period. After a training period required to learn the procedure, mice were randomly subjected to a bottle containing a control solution (mineral oil; Cooper, France) or a bottle containing an experimental one [mineral oil + 0.5% oleic acid (OLA); Sigma-Aldrich] for 15 min. Then mice were offered the other bottle for an additional 15 min session. In this experiment, data were analyzed for 1 or 5 min from the first lick to exclude postingestive signals. OLA was chosen because it is the main LCFA found in rapeseed oil. CVP from fasted control and DIO mice were fixed for 3 h in ice-cold 4% paraformaldehyde in 0.1 M phosphate buffer, pH 7.4. Samples were cryoprotected by incubation in 15% sucrose in 0.1 M phosphate buffer for 2 h, followed by overnight treatment with 30% sucrose in phosphate buffer. CVP were then embedded in OCT medium (Tissue-Tek; Sakura Finetek) and stored at −80°C. Cryostat sections (10 µm) were air dried for 45 min at room temperature and rehydrated in 0.1 M PBS (pH 7.4) for 10 min. Rehydrated sections were blocked in 10% FA-free BSA and 0.2% Triton X-100 in PBS for 1 h at room temperature and incubated overnight at 4°C with a polyclonal anti-rabbit CD36 antibody (1:50; Abcam ab80978). After washing, sections were incubated for 3 h at room temperature with a fluorescent anti-rabbit secondary antibody (Alexa 568, 1:200 dilution; Invitrogen) and then counterstained with Hoechst reactive (0.05 mg/ml; Sigma-Aldrich) to stain the nuclei. Slices were analyzed under an epifluorescent microscope (Axiovert 200M). No fluorescent staining was observed when the primary antibody was omitted. Freshly isolated mouse CVP were homogenized using a micro-potter in a TSE buffer [50 mM Tris HCl, 150 mM NaCl, 1 mM EDTA, 1% Igepal CA-630, 5 µl/ml anti-protease cocktail (Sigma-Aldrich), and 100 µl/10 ml antiphosphatase (Thermo Fischer)]. Samples were stored on ice for 30 min and then centrifuged (12,000 g, 15 min, 4°C). Lysates were used immediately or stored at −80°C until the assay. Protein concentrations in homogenates were assayed using a BCA kit (Thermo Fisher). Denaturated proteins (4 µg) were separated by SDS-PAGE (10%) and transferred to a polyvinylidene difluoride membrane by electroblotting. After being blocked overnight using a TBS buffer containing 5% BSA and 0.05% Tween-20, membranes were incubated for 3 h with an anti-CD36 antibody (1:1,000 dilution; R and D Systems). After a set of washes, the appropriate peroxidase-conjugated secondary antibody was added. Antibody labeling was detected by chemiluminescence (ECL-plus reagent; Perkin Elmer). β-Actin (1:100 dilution; Santa Cruz) was used as an internal reference protein. Each point corresponds to a pool of total proteins from three mice CVP. Each experiment was repeated three times. CD36-positive taste buds cells were freshly isolated from mouse CVP as described previously (8El-Yassimi A. Hichami A. Besnard P. Khan N.A. Linoleic acid induces calcium signaling, Src kinase phosphorylation, and neurotransmitter release in mouse CD36-positive gustatory cells.J. Biol. Chem. 2008; 283: 12949-12959Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 10Gaillard D. Laugerette F. Darcel N. El-Yassimi A. Passilly-Degrace P. Hichami A. Khan N.A. Montmayeur J.P. Besnard P. The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse.FASEB J. 2008; 22: 1458-1468Crossref PubMed Scopus (181) Google Scholar) and further cultured for 24 h in Willico-Dish wells containing RPMI-1640 medium, supplemented with 10% fetal calf serum, 200 U/ml penicillin, and 0.2 mg/ml streptomycin. The following day, the CD36-positive taste bud cells were gently washed with a buffer containing the following: 3.5 mM KH2PO4; 17.02 mM Na2HPO4; 136 mM NaCl, pH 7.4. The cells were then incubated with Fura-2/AM (1 µM) for 60 min at 37°C in loading buffer that contained the following: 110 mM NaCl; 5.4 mM KCl; 25 mM NaHCO3; 0.8 mM MgCl2; 0.4 mM KH2PO4; 20 mM Hepes-Na; 0.33 mM Na2HPO4; 1.2 mM CaCl2, pH 7.4. After loading, the cells (2 × 106/ml) were washed three times and remained suspended in the identical buffer. The changes in intracellular Ca2+ (F340/F380) were monitored under the Nikon microscope (TiU) by using an S-fluor 40× oil immersion objective. The planes were taken at Z intervals of 0.3 μm, and NIS-Elements software was used to deconvolve the images. The microscope was equipped with an EM-CCD (Lucas) camera for real-time recording of 16 bit digital images. The dual excitation fluorescence imaging system was used for studies of individual cells. The changes in intracellular Ca2+ were expressed as ΔRatio, which was calculated as the difference between the peak F340/F380 ratio. The data were summarized from the large number of individual cells (20–40 cells in a single run, with three to nine identical experiments done in at least three cell preparations). For experiments in Ca2+−free medium, CaCl2 was replaced by EGTA (2 mM). Each point corresponds to a pool of total proteins from 25 mice CVP. Each experiment was repeated three times. Results are expressed as mean ± SEM. The significance of differences between groups was evaluated with XLSTAT (Addinsoft; France). We first checked that the data for each group were normally distributed and that variances were equal. We then carried out two-tailed Student's t-tests, Mann-Whitney tests, or Pearson correlation. To explore whether the preference for lipid-rich foods might be affected by eating habits leading to obesity, mice were chronically fed obesogenic diets (Table 1). As expected, animals chronically subjected to the HF diet rapidly developed obesity (Fig. 1A). A 2- and 3-fold increase in fat mass was found after 4 and 23 weeks of diet, respectively. Fasted plasma glucose levels and insulinemia were also enhanced in DIO mice, suggesting the development of insulin resistance at only 4 weeks of treatment (Fig. 1B). Long-term (12 h) two-bottle preference tests performed in control mice subjected to different concentrations of rapeseed oil (0.01–2.0% w/v) established that animals were able to detect and prefer oily solution when lipid concentration reached 0.02% in emulsion, the maximal preference being observed with 2.0% oil (13Martin C. Passilly-Degrace P. Chevrot M. Ancel D. Sparks S.M. Drucker D.J. Besnard P. Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity.J. Lipid Res. 2012; 53: 2256-2265Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar). In contrast to controls, DIO mice were unable to properly detect a low concentration of oil (0.02%) whatever the duration of the treatment (4 and 23 weeks). Moreover, mice fed a HF diet for 4 or 23 weeks showed a lower attraction for 2.0% oily solution than controls (Fig. 1C). Altogether, these data indicate that the chronic consumption of HF diet increases the detection threshold (decreased sensitivity) for lipids. Similar results were obtained when mice were chronically fed another obesogenic diet [high–fat/high-sucrose (HFHS) diet, supplementary data I], suggesting that it is the induction of obesity, rather than the qualitative diet composition, that might be the major determinant of this behavioral change. To explore whether this relative orosensory indifference to dietary lipids was related to the fat mass, mice fed the HF diet ad libitum for 4 weeks were then subjected to a caloric restriction [i.e., 60% (w/w) of the previous HF diet consumption] until their fat mass returned to control values (Fig. 2A). Comparative analysis of preference tests performed during the weight gain/weight loss sequence revealed that the preference for lipids was tightly related to fat mass in the mouse. Indeed, mice fed the calorie-restricted diet displayed a behavior similar to that of controls maintained on regular chow, with a greater preference for 0.2% and 2.0% oil than that found when they were obese (Fig. 2B). A significant inverse correlation between attraction for fat and adiposity was found (Fig. 2C). A similar association was also found in HFHS-fed mice subjected to the licking paradigm. Indeed, the preference for OLA, determined using brief (5 min) computer-controlled licking tests and the fat mass accumulation assayed by echo-MRI, supports the fact that orosensory detection of lipids is dependent on adipose tissue size (Fig. 2D). Although most taste bud cells express insulin receptor (20Suzuki Y. Takeda M. Sakakura Y. Suzuki N. Distinct expression pattern of insulin-like growth factor family in rodent taste buds.J. Comp. Neurol. 2005; 482: 74-84Crossref PubMed Scopus (14) Google Scholar), obesity-associated insulin resistance does not play a role in the preference for oily solution. Indeed, no correlation between plasma insulin levels and fat preference was found in controls, DIO, or DIO-restricted mice (Fig. 3).Fig. 3Correlation between plasma insulin levels and preference for fat. Experiments were performed in controls, DIO, and energy-restricted DIO mice subjected to two-bottle preference tests in the presence of various concentrations of rapeseed oil. Dotted line represents the absence of preference. Plasma insulin levels were assayed using a commercial kit.View Large Image Figure ViewerDownload Hi-res image Download (PPT) In gustatory mucosa, CD36 is thought to be a lipid receptor implicated in the orosensory detection of dietary lipids (i.e., LCFA). To determine whether the lower lipid preference found in obese mice was related to lingual CD36 protein, comparison of immunolocalization of CD36 was undertaken in CVP from overnight-fasted controls and DIO mice. As shown in Fig. 4A, CD36 displays the same expression pattern in obese as in control mice. To confirm this observation, Western blotting analysis was performed in CVP. Similar expression levels of CD36 were found in control and obese mice, whatever the duration of HF diet (Fig. 4B) or the composition of obesogenic diet used (HFHS - supplementary data II). It was recently reported in mouse CVP that CD36 protein levels are downregulated by lipids during the postprandial period (11Martin C. Passilly-Degrace P. Gaillard D. Merlin J.F. Chevrot M. Besnard P. The lipid-sensor candidates CD36 and GPR120 are differentially regulated by dietary lipids in mouse taste buds: impact on spontaneous fat preference.PLoS ONE. 2011; 6: e24014Crossref PubMed Scopus (127) Google Scholar), and a disturbance in this regulation affects the spontaneous attraction for fat (13Martin C. Passilly-Degrace P. Chevrot M. Ancel D. Sparks S.M. Drucker D.J. Besnard P. Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity.J. Lipid Res. 2012; 53: 2256-2265Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar). Therefore, it was tempting to speculate that the lower attractive effect of oily solutions found in obese mice might be due to a dysfunction in this regulatory loop controlling the amounts of CD36 in CVP during a meal. To explore this hypothesis, CD36 protein levels in CVP were compared in fasted and refed controls and DIO mice. Because CD36 in CVP is lipid sensitive and its postprandial decrease is significant 60 min after the beginning of a meal (11Martin C. Passilly-Degrace P. Gaillard D. Merlin J.F. Chevrot M. Besnard P. The lipid-sensor candidates CD36 and GPR120 are differentially regulated by dietary lipids in mouse taste buds: impact on spontaneous fat preference.PLoS ONE. 2011; 6: e24014Crossref PubMed Scopus (127) Google Scholar), animals were refed the HF diet for 1 h. Consistent with data shown in Fig. 4B, fasted controls and DIO mice displayed similar CD36 expression levels in CVP. By contrast, the drop in CD36 content of CVP found 1 h after refeeding in controls was not retrieved in obese mice (Fig. 4C). In mouse CVP, LCFA-mediated activation of CD36 triggers a complex signaling cascade, producing a huge rise in intracellular free calcium concentrations ([Ca2+]i) at the origin of neurotransmitters release (8El-Yassimi A. Hichami A. Besnard P. Khan N.A. Linoleic acid induces calcium signaling, Src kinase phosphorylation, and neurotransmitter release in mouse CD36-positive gustatory cells.J. Biol. Chem. 2008; 283: 12949-12959Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 9Dramane G. Abdoul-Azize S. Hichami A. Vogtle T. Akpona S. Chouabe C. Sadou H. Nieswandt B. Besnard P. Khan N.A. STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice.J. Clin. Invest. 2012; 122: 2267-2282Crossref PubMed Scopus (62) Google Scholar–10Gaillard D. Laugerette F. Darcel N. El-Yassimi A. Passilly-Degrace P. Hichami A. Khan N.A. Montmayeur J.P. Besnard P. The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse.FASEB J. 2008; 22: 1458-1468Crossref PubMed Scopus (181) Google Scholar). To assess whether obesity-mediated decrease in fat preference is due to a dysfunction in the CD36-dependent signaling, calcium imaging experiments were performed on freshly purified CD36-positive taste bud cells from control or from mice fed the HF for 4 weeks. The effects of the two main LCFAs present in rapeseed oil, i.e., linoleic acid (LA) and OLA, were studied. Consistent with previously published data (8El-Yassimi A. Hichami A. Besnard P. Khan N.A. Linoleic acid induces calcium signaling, Src kinase phosphorylation, and neurotransmitter release in mouse CD36-positive gustatory cells.J. Biol. Chem. 2008; 283: 12949-12959Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 10Gaillard D. Laugerette F. Darcel N. El-Yassimi A. Passilly-Degrace P. Hichami A. Khan N.A. Montmayeur J.P. Besnard P. The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse.FASEB J. 2008; 22: 1458-1468Crossref PubMed Scopus (181) Google Scholar), addition of LA or OLA led to a rapid rise in [Ca2+]i in taste bud cells from control mice (Fig. 5A). LCFA-evoked rise in [Ca2+]i in a medium containing calcium (100% Ca2+) was found to be decreased, albeit to a lesser extent, in the absence of calcium (0% Ca2+), suggesting that LCFA led to the recruitment of calcium from both extra- and intracellular pools (Fig. 5A). Although taste bud cells isolated from CVP of obese mice were responsive to LA or OLA (Fig. 5B), [Ca2+]i rises were dramatically lower than those found in CVP from lean controls in 0 or 100% calcium media (Fig. 5C). Obesity is one of the major public health challenges in the world by reason of the deleterious effects of its associated diseases (i.e., type 2 diabetes, vascular disorders, hypertension, cancer). Although the origin of the obesity epidemic is clearly multi-factorial, eating habits, especially overconsumption of high-palatable energy-dense foods, are thought to play a significant role in this situation (4Drewnowski A. Greenwood M.R. Cream and sugar: human preferences for high-fat foods.Physiol. Behav. 1983; 30: 629-633Crossref PubMed Scopus (299) Google Scholar). Several lines of evidence indicate that laboratory rodents and humans display a" @default.
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• W2150804024 title "Obesity alters the gustatory perception of lipids in the mouse: plausible involvement of lingual CD36" @default.
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