Academic literature on the topic 'Bitter taster receptor'
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Journal articles on the topic "Bitter taster receptor"
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Feeney, E., S. O'Brien, A. Scannell, A. Markey, and E. R. Gibney. "Genetic variation in taste perception: does it have a role in healthy eating?" Proceedings of the Nutrition Society 70, no. 1 (November 22, 2010): 135–43. http://dx.doi.org/10.1017/s0029665110003976.
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Taste is often cited as the factor of greatest significance in food choice, and has been described as the body's ‘nutritional gatekeeper’. Variation in taste receptor genes can give rise to differential perception of sweet, umami and bitter tastes, whereas less is known about the genetics of sour and salty taste. Over twenty-five bitter taste receptor genes exist, of which TAS2R38 is one of the most studied. This gene is broadly tuned to the perception of the bitter-tasting thiourea compounds, which are found in brassica vegetables and other foods with purported health benefits, such as green tea and soya. Variations in this gene contribute to three thiourea taster groups of people: supertasters, medium tasters and nontasters. Differences in taster status have been linked to body weight, alcoholism, preferences for sugar and fat levels in food and fruit and vegetable preferences. However, genetic predispositions to food preferences may be outweighed by environmental influences, and few studies have examined both. The Tastebuddies study aimed at taking a holistic approach, examining both genetic and environmental factors in children and adults. Taster status, age and gender were the most significant influences in food preferences, whereas genotype was less important. Taster perception was associated with BMI in women; nontasters had a higher mean BMI than medium tasters or supertasters. Nutrient intakes were influenced by both phenotype and genotype for the whole group, and in women, the AVI variation of the TAS2R38 gene was associated with a nutrient intake pattern indicative of healthy eating.
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Abrol, Ravinder, Jun Tan, Hongxiang Hui, William A. Goddard III, and Stephen J. Pandol. "Structural basis for bitter taste receptor activation and its potential role in targeting diabetes." Functional Foods in Health and Disease 5, no. 3 (March 18, 2015): 117. http://dx.doi.org/10.31989/ffhd.v5i3.176.
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Background: Taste receptors are G protein-coupled receptors that, besides being present in the taste buds, have also been shown to be present in the gastrointestinal (GI) system, respiratory system, and brain, though their function at these locations is not well understood.Objective: To understand the nutrient mediated release of gut peptides like GLP-1 from enteroendocrine L-cells of the GI system, we focused on a bitter taste receptor TAS2R38 (based on animal models) to investigate the structural basis of its potential role in the release of gut peptides. Methods: The atomic-level structure of bitter taste receptor TAS2R38 was predicted using GEnSeMBLE, a first-principle based GPCR structure prediction method. These structures were obtained for the dominant taster haplotype (PAV) as well as for the nontaster haplotype (AVI) of the receptor. The known ligands phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PTU) were docked to these structures to provide a structural basis for the taster and nontaster haplotypes.Results: Docking of known ligands PTU and PTC to taster and nontaster haplotypes of the bitter taste receptor showed a backbone hydrogen bond to residue 262 in taster but not in nontaster haplotype, suggesting a potential mode of action of these molecules in the activation of the bitter taste receptor. Conclusion: These results, combined with the ability of PTC to release gut peptides from in vitro models of the enteroendocrine L-cells, suggest a potential structural basis for TAS2R38 activation that can lead to the release of those peptides. This release has a therapeutic benefit for type 2 diabetes and implies a role for bitter tasting (but safe) natural compounds targeting TAS2R38 as potential drug candidates for curing type 2 diabetes.Key words: TAS2R38, GLP-1 release, PYY release, CCK release, enteroendocrine L cell, GPCR, protein structure prediction, GEnSeMBLE
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Pilic, Leta, Catherine Anna-Marie Graham, Nisrin Hares, Megan Brown, Jonathan Kean, Yasmin Wehliye, Ella McGrigor, et al. "Bitter Taste Sensitivity Is Determined by TAS2R38 Haplotype, Associated with Saturated Fat Intake and Is Lower in Overweight and Obese Compared to Normal Weight UK adults." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1271. http://dx.doi.org/10.1093/cdn/nzaa058_029.
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Abstract Objectives Taste perception (sensitivity) may be determined by genetic variations in taste receptors and it affects food intake. Lower fat taste sensitivity is associated with higher dietary fat intake and body mass index (BMI). Recently, associations between bitter and fat taste sensitivity have been reported whereby bitter taste perception may be involved in textural perception of dietary fat. However, it is not clear if lower sensitivity to bitter taste would lead to an actual higher fat intake. Our objectives were to explore the associations between haplotypes in the bitter taste receptor TAS2R38, bitter taste sensitivity and fat intake and if bitter taste sensitivity is lower in individuals with higher BMI. Methods Ethical approval was obtained from the St Mary's and Oxford Brookes University Ethics Committee. Eighty-eight healthy Caucasian participants (44% male and 56% female; mean BMI 24.9 ± 4.8 kg/m2 and mean age 35 ± 14 years) completed this cross-sectional study. Height and weight were measured and genotyping performed for rs713598, rs1726866, rs10246939 genetic variants in the TAS2R38. Haplotypes were determined with Haploview software. Participants rated the intensity of a phenylthiocarbamide (PTC) impregnated strip on the general Labelled Magnitude Scale (gLMS) to determine bitter taste sensitivity and were classified as bitter tasters and non-tasters. Dietary fat intake was calculated from the EPIC-Norfolk Food Frequency Questionnaire and expressed as % total energy intake. Results TAS2R38 haplotypes were associated with bitter taster status (P < 0.005). PTC ratings of intensity were negatively correlated with % saturated fat (SFA) intake (rs = −0.256, P = 0.016). %SFA and %total fat (rs = 0.656, P < 0.005) and %total fat and energy intake (kcal) (rs = 0.225, P = 0.035) were positively correlated. Normal weight participants rated PTC strips as more intense compared to overweight and obese participants (mean rank 53 vs. 41, P = 0.033). Conclusions Bitter taste perception is determined by genetics and lower sensitivity to this taste is associated with higher intake of SFA. Lower bitter taste sensitivity in overweight/obese participants suggests that impaired bitter taste may be associated with an overall unhealthier and more energy dense dietary pattern. Funding Sources St Mary's and Oxford Brookes University.
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Biró, Barbara, Dániel Koren, Adrienn Lichthammer, Márta Veresné Bálint, Attila Gere, and Zoltán Kókai. "Relationships amongst phenyltiocarbamide sensitivity, body composition, coffee and tea consumption." Élelmiszervizsgálati Közlemények 68, no. 2 (2022): 3855–65. http://dx.doi.org/10.52091/evik-2022/2-1-eng.
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Polymorphisms of TAS2R38 gene responsible for bitter taste perception elicit a bimodal receptor response in the population upon the detection of phenylthiocarbamide and 6-n-propylthiouracil, respectively. Genetic differences in sensitivity to phenylthiocarbamide and 6-n-propylthiouracil may affect body composition, food preferences, and frequency of consuming different food types. To date, no publication has been published in Hungary on the joint study of these factors. The aim of the present research is to find correlations between phenylthiocarbamide taster status and body composition, and the frequency of consumption of different bitter-tasting foods. In the study, a taster status survey of participants (n = 170), a bioimpedance-based body composition analysis (n = 96) and completed a food frequency questionnaire of bitter foods (n = 170) were conducted. Descriptive statistical methods, cross-tabulation analysis, multiple correspondence analysis, and Mann-Whitney test were used for data analysis at 5% significance level. The proportions of the taster and non-taster categories proved to be the same as reported by international literature (70%/30% respectively). There were no significant correlations among taster status and the other examined parameters, however, based on the multiple correspondence analysis, the observed trends are in accordance with the international literature. There were significant correlations among gender, body composition and some variables describing food preference. Based on the literature data and our own results, there can be a relationship between genotype and body composition, and genotype and food choice. Further analyses with large-sample size and representative research are needed to substantiate these assumptions.
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Ergün, Can, and Meral Aksoy. "Relationships between the hTAS2R38 genotype, food choice, and anthropometric variables in normal-weighted and overweight adults." Genetika 45, no. 2 (2013): 381–91. http://dx.doi.org/10.2298/gensr1302381e.
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Aim: Taste is a major determinant of food choice; however, there is a great lack of knowledge about how taste perception affects human nutrition. Bitter taste perception presents unique opportunities for investigating this subject. The aim of this study was to determine whether polymorphisms on the bitter taste receptor gene hTAS2R38 affect an individual?s food choices and some anthropometric variables. Subjects and Method: In this study, the possible relationship between food preferences, body weight, and polymorphisms on hTAS2R38 was investigated in healthy volunteers (n=178) who weighed within the normal range (BMI: 20-24.9 kg/m2, n=90) and those who were overweight, but otherwise healthy (BMI ? 25.0 kg/m2, n=88). Descriptive information about the subjects was collected via a questionnaire, and anthropometric measurements were taken by the researcher. Records of three consecutive days of food consumption were collected to determine each subject?s macronutrient intake. For identification of the hTAS2R38 genotype, samples were taken from each participant's in-mouth epithelial cell line, and the genetic material was analyzed at the laboratory for Rs713598. Results: The percentage of ?non-tasters? (n=42) among the whole population was 23.6% (C-Homozygote: 23.6%) while ?tasters? (n=136) comprised 76.4% (CG-Heterozygote: 46.6%, G-Homozygote: 29.8%). When group-wide and between-group comparisons were made, it was revealed that taster status didn?t affect differences in anthropometric measures. Detected differences in macronutrient intake were due to gender. Discussion: Polymorphisms on hTAS2R38 bitter taste receptor gene had no effect on variables such as body weight, anthropometric variables, body fat percentage, or food choices within the study population.
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INOUE, MASASHI, XIA LI, STUART A. McCAUGHEY, GARY K. BEAUCHAMP, and ALEXANDER A. BACHMANOV. "Soa genotype selectively affects mouse gustatory neural responses to sucrose octaacetate." Physiological Genomics 5, no. 4 (April 27, 2001): 181–86. http://dx.doi.org/10.1152/physiolgenomics.2001.5.4.181.
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In mice, behavioral acceptance of the bitter compound sucrose octaacetate (SOA) depends on allelic variation of a single gene, Soa. The SW.B6- Soabcongenic mouse strain has the genetic background of an “SOA taster” SWR/J strain and an Soa-containing donor chromosome fragment from an “SOA nontaster” C57BL/6J strain. Using microsatellite markers polymorphic between the two parental strains, we determined that the donor fragment spans 5–10 cM of distal chromosome 6. The SWR/J mice avoided SOA in two-bottle tests with water and had strong responses to SOA in two gustatory nerves, the chorda tympani (CT) and glossopharyngeal (GL). In contrast, the SW.B6- Soab mice were indifferent to SOA in two-bottle tests and had very weak responses to SOA in both of these nerves. The SWR/J and SW.B6- Soab mice did not differ in responses of either nerve to sucrose, NaCl, HCl, or the bitter-tasting stimuli quinine, denatonium, strychnine, 6- n-propylthiouracil, phenylthiocarbamide, and MgSO4. Thus the effect of the Soa genotype on SOA avoidance is mediated by peripheral taste responsiveness to SOA, involving taste receptor cells innervated by both the CT and GL nerves.
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Taha, Mohamed A., Christian A. Hall, Colin J. Shortess, Richard F. Rathbone, and Henry P. Barham. "Treatment Protocol for COVID-19 Based on T2R Phenotype." Viruses 13, no. 3 (March 18, 2021): 503. http://dx.doi.org/10.3390/v13030503.
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COVID-19 has become a global pandemic of the highest priority. Multiple treatment protocols have been proposed worldwide with no definitive answer for acure. A prior retrospective study showed association between bitter taste receptor 38 (T2R38) phenotypes and the severity of COVID-19. Based on this, we proposed assessing the different T2R38 phenotypes response towards a targeted treatment protocol. Starting July 2020 till December 2020, we tested subjects for T2R38 phenotypic expression (supertasters, tasters, and nontasters). Subjects who were subsequently infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (diagnosed via PCR) were included. Based on their taster status, supertasters were given dexamethasone for 4 days; tasters were given azithromycin and dexamethasone +/− hydroxychloroquine for 7 days; and nontasters were given azithromycin and dexamethasone for 12 days. Subjects were followed prospectively and their outcomes were documented. Seven hundred forty-seven COVID-19 patients were included, with 184 (24.7%) supertasters, 371 (49.6%) tasters, and192 (25.7%) nontasters. The average duration of symptoms with the treatment protocol was 5 days for supertasters, 8.1 days for tasters, and 16.2 days for nontasters. Only three subjects (0.4%) required hospitalization (3/3 nontasters). Targeted treatment protocol showed significant correlation (p < 0.05) based on patients’ T2R38 phenotypic expression. Assessing treatment protocols for COVID-19 patients according to their T2R38 phenotype could provide insight into the inconsistent results obtained from the different studies worldwide. Further study is warranted on the categorization of patients based on their T2R38 phenotype.
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Deshaware, Shweta, and Rekha Singhal. "Genetic variation in bitter taste receptor gene TAS2R38 , PROP taster status and their association with body mass index and food preferences in Indian population." Gene 627 (September 2017): 363–68. http://dx.doi.org/10.1016/j.gene.2017.06.047.
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Lemon, Christian H., and David V. Smith. "Neural Representation of Bitter Taste in the Nucleus of the Solitary Tract." Journal of Neurophysiology 94, no. 6 (December 2005): 3719–29. http://dx.doi.org/10.1152/jn.00700.2005.
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Based on the molecular findings that many bitter taste receptors (T2Rs) are expressed within the same receptor cells, it has been proposed that bitter taste is encoded by the activation of discrete neural elements. Here we examined how a variety of bitter stimuli are represented by neural activity in central gustatory neurons. Taste responses (spikes/s) evoked by bathing the tongue and palate with intensity-matched concentrations (in M) of 2 sugars (0.32 sucrose and 0.5 D-fructose), ethanol (40%), 4 salts (0.01 NaCl, 0.008 NaNO3, 0.01 MgCl2, and 0.05 KCl), 2 acids (0.003 HCl and 0.005 citric acid), and 10 bitter ligands (0.007 quinine-HCl, 0.015 denatonium benzoate, 0.003 l-cysteine, 0.001 nicotine, 0.005 strychnine-HCl, 0.04 tetraethylammonium chloride, 0.03 atropine-SO4, 0.005 brucine-SO4, 0.03 papaverine-HCl, and 0.009 sparteine) were recorded from 51 neurons in the nucleus of the solitary tract of anesthetized rats. Cluster analysis was used to categorize neurons into types based on responses to sucrose, NaCl, HCl, and quinine-HCl. Three groupings emerged: type S (responded optimally to sweets), type N (sodium-optimal), and type H/Q (responded robustly to bitters, acids, and salts). Multivariate analyses revealed that across-neuron patterns of response among bitter stimuli were strongly correlated. However, neural type H/Q, which was most responsive to bitter tastants, was not differentially sensitive to bitter stimuli and Na+ salts, which rats perceive as distinct. Thus central neurons most responsive to bitter substances receive significant input from receptors that mediate other tastes, indicating that bitter stimuli are not represented by activity in specifically tuned neurons.
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Schiffman, SS. "Taste Transduction and Modulation." Physiology 3, no. 3 (June 1, 1988): 109–12. http://dx.doi.org/10.1152/physiologyonline.1988.3.3.109.
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The application to the tongue of agents that interact with taste cells can tell us a great deal about transduction mechanisms that mediate taste. Separate pathways for Na+ and K+ appear to be part of the transduction mechanisms for the tastes of sodium and potassium salts. Caffeine and other methyl xanthines can potentiate certain tastes;this enhancement may involve the interaction of caffeine with an adenosine receptor. There is also evidence for glutamate and inosine receptors in addition to multiple receptors for sweet and bitter tastes.
Dissertations / Theses on the topic "Bitter taster receptor"
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Clapp, Tod R. "Characterization of IP₃ receptors in bitter taste transduction." Access citation, abstract and download form; downloadable file 3.78 Mb, 2004. http://wwwlib.umi.com/dissertations/fullcit/3131664.
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Johnson, Claire. "Sensory and chemical analysis of the bitter-sweet taste interaction." Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262530.
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Pydi, Sai Prasad. "Structural and functional characterization of bitter taste receptors, T2R1 and T2R4." American Society for Biochemistry and Molecular Biology, 2011. http://hdl.handle.net/1993/23607.
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In humans, taste is one of the five senses, and helps in the recognition of nutritionally important and potentially harmful substances. It triggers innate behaviour to accept or reject food. Humans can sense five basic tastes, which are sweet, umami, bitter, salt and sour. The receptors that mediate bitter, sweet and umami tastes belong to the G protein-coupled receptor (GPCR) superfamily. A group of three receptors sense sweet and umami tastes, whereas bitter taste is sensed by 25 bitter taste receptors (referred as T2Rs). T2Rs are activated by structurally diverse natural and synthetic bitter compounds. Many common pharmaceutical compounds are bitter in taste and these are effective ligands for T2Rs. Recent finding of T2Rs in extra-oral tissues suggests these receptors are also involved in various physiological and pathophysiological processes. To understand the structure and function of these receptors, studies directed at elucidating their mechanisms of activation, and identification of novel ligands including bitter blockers (antagonists and inverse agonists), are required.
To obtain mechanistic insights into the role of the highly conserved, and receptor specific residues, two bitter taste receptors (T2R1 and T2R4) were targeted. In this study, a combination of molecular, biochemical and pharmacological approaches were used to identify the amino acids and motifs, important for T2Rs to switch from inactive to active state. A hydrogen-bonding network between transmembrane (TM) helices 1-2-7 was identified as important for T2R activation. Alanine-scan mutagenesis of intracellular loops (ICLs) 2 and 3 identified T2R regions important for G protein binding, and receptor activation. A pharmacological method was developed, to screen potential bitter blockers for T2Rs. Using this method, three novel bitter blockers, which include two natural antagonists and one synthetic inverse agonist for T2R4, were discovered. The role of expression tags in enhancing T2R4 expression was also pursued. T2R4 expression on the cell surface was increased 2.5 fold, when its N-terminus was tagged with rhodopsin N-terminal 33 residues (Rho33- T2R4 chimera). In conclusion, work carried out provides novel insights into the mechanisms of T2R activation, and in the discovery of bitter blockers for T2R4.
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Bufe, Bernd. "Identifizierung und Charakterisierung von Bitterrezeptoren." Phd thesis, [S.l.] : [s.n.], 2003. http://pub.ub.uni-potsdam.de/2004/0013/bufe.pdf.
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Brissard, Léa. "Mechanisms of gustatory perception of dietary lipids : cross-talk with bitter taste and endocannabinoid receptors." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCK071/document.
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L'obésité constitue l'un des principaux problèmes de santé publique en ce début du 21ème siècle. Sa prévalence augmente régulièrement, en particulier chez les enfants. Ce constat n'est pas anodin car l'obésité est généralement associée à diverses pathologies graves (diabète de type 2, hypertension et cancer,…). Ainsi, des investigations sur les mécanismes impliqués dans la perception gustative des lipides alimentaires pourraient éclairer leurs rôles dans l’incidence de l’obésité.Plusieurs études ont démontré le rôle des endocannabinoïdes et des aliments amers dans l’obésité. Ainsi, nous avons étudié l’interaction (cross-talk) des récepteurs cannabinoïdes et du goût amer avec le goût lipidique. Cette thèse comporte ainsi deux volets : les récepteurs cannabinoïdes (CB1R), le goût amer et leurs interactions avec les récepteurs lipidiques.Dans la première partie, nous avons étudié le rôle régulateur de CB1R. Dans la présente étude, des tests comportementaux sur des souris CB1R-/- et des souris de type sauvage (WT) ont montré que l'invalidation du gène Cb1r était associée à une faible préférence pour les solutions contenant de l'huile de colza ou un acide gras à longue chaîne (AGLC) tel que l’acide linoléique (LA). L'administration de rimonabant, un agoniste-inverse de CB1R, chez la souris a également entraîné une faible préférence pour les acides gras alimentaires. Aucune différence dans l'expression des protéines CD36 et GPR120 n'a été observée dans les cellules des papilles gustatives des souris WT et CB1R-/-. La signalisation calcique via CD36 dans les cellules des papilles gustatives des souris CB1R-/- diminue de façon significative par rapport à celle observée dans les cellules gustatives des souris WT. Les cellules des papilles gustatives des souris CB1R-/- présentent également une diminution significative de l'ARNm de Pro-glucagon et de Glp-1r et un faible niveau basal de GLP-1. Nous rapportons que CB1R est impliqué dans la perception du goût du gras via la signalisation calcique et la sécrétion de GLP-1.Dans la seconde partie, nous avons d’abord caractérisé le phénotype de cellules fongiformes humaines (HTC-8). En effet, le projet de ma thèse comprend la caractérisation à l’échelle moléculaire des récepteurs amers et lipidiques et leur cross-talk dans ces cellules (collaboration BRAIN, Allemagne). Nous avons démontré que les cellules HTC-8 expriment PLCβ2 et l’α-gustducin à l’échelle des ARNm et des protéines. Elles expriment également TAS2R16 et TAS2R38 et ces mêmes cellules co-expriment CD36 et GPR120. Puis, nous avons étudié la signalisation via ces récepteurs en utilisant l’acide linoléique, un agoniste de CD36 et GPR120, la sinigrin, agoniste de TAS2R16 et TAS2R38, la salicin, agoniste du récepteur TAS2R16 et le phénylthiocarbamide, agoniste du récepteur TAS2R38. De plus, les études du signal calcique ont démontré que la signalisation en aval du goût gras partage une voie commune avec la signalisation en aval du goût amer, mettant en évidence un cross-talk entre ces deux modalités gustatives.Bien que nous ayons montré le cross-talk entre les modalités gustatives amère et lipidique, il nous reste à étudier ces phénomènes à l’échelle de l’organisme. Ces résultats, d’ores et déjà, montrent que le goût amer et le récepteur cannabinoïde-1 sont liés à la sensibilité au goût du gras et doivent être pris en compte pour la gestion de l'obésitéObesity is one of the major public health problems at the beginning of the 21st century. Its prevalence is increasing steadily, especially among children. This observation is not insignificant because obesity is generally associated with various serious pathologies (type 2 diabetes, hypertension and cancer, etc.). Thus, investigations into the mechanisms involved in the taste perception of dietary lipids could shed light on their roles in the incidence of obesity.Several studies have demonstrated the role of endocannabinoids and bitter foods in obesity. Thus, we studied the cross-talk of cannabinoid receptors and bitter taste with lipid taste. This thesis has two components: cannabinoid receptors (CB1R), bitter taste and their interactions with lipid receptors.In the first part, we studied the regulatory role of CB1R. In the present study, behavioral tests on CB1R-/- mice and wild-type (WT) mice showed that the invalidation of the Cb1r gene was associated with a low preference for solutions containing rapeseed oil or a long chain fatty acid (LCFA) such as linoleic acid (LA). Administration of rimonabant, a CB1R inverse agonist, in mice also resulted in a low preference for dietary fatty acids. No differences in the expression of CD36 and GPR120 proteins were observed in the taste buds cells of the WT and CB1R-/- mice. Calcium signaling via CD36 in the taste bud cells of CB1R-/- mice decreased significantly compared with those observed in the taste cells of WT mice. The taste bud cells of CB1R-/- mice also show a significant decrease in Pro-glucagon and Glp-1r mRNA and a low basal level of GLP-1. We report that CB1R is involved in the perception of fat taste via calcium signaling and secretion of GLP-1.In the second part, we first characterized the phenotype of human fungiform cells (HTC-8). Indeed, the project of my thesis includes the characterization on the molecular scale of bitter and lipid receptors and their cross-talk in these cells (collaboration BRAIN, Germany). We have demonstrated that HTC-8 cells express PLCβ2 and α-gustducin at the mRNA and protein level. They also express TAS2R16 and TAS2R38 and these same cells co-express CD36 and GPR120. Then, we studied signaling via these receptors using linoleic acid, a CD36 and GPR120 agonist, sinigrin, TAS2R16 agonist and TAS2R38, salicin, TAS2R16 receptor agonist, and phenylthiocarbamide, TAS2R38 receptor agonist. In addition, calcium signal studies have shown that downstream fatty signaling shares a common path with downstream bitter taste signaling, highlighting a cross-talk between these two taste modalities.Although we have shown the cross-talk between bitter and lipid taste modalities, we still have to study these phenomena at the level of the organism. These results, already, show that the bitter taste and the cannabinoid-1 receptor are related to the taste sensitivity of fat and must be taken into account for the management of obesity
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Grau, Bové Maria Carme. "Regulation of enteroendocrine function by bioactive components through their interaction with bitter taste receptors." Doctoral thesis, Universitat Rovira i Virgili, 2021. http://hdl.handle.net/10803/672967.
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El sistema enteroendocrí es troba al tracte gastrointestinal i controla la gana i l’activitat pancreàtica endocrina, entre
altres funcions. Els compostos bioactius que estimulen aquest sistema són candidats terapèutics per tractar patologies
relacionades amb aquestes funcions. Prèviament s’ha identificat que un extracte de proantocianidines de llavors de
raïm (GSPE) és antidiabètic per les seves capacitats de millora de la funció de les cèl·lules i la seva capacitat
saciant, com a conseqüència en part de l’activació del sistema enteroendocrí. El nostre grup ha relacionat les
secrecions enteroendocrines induïdes per polifenols amb l'estimulació de receptors del gust amarg (TAS2R) in vitro,
però si això es reflecteix en una ingesta alterada encara és deconegut. Per això, és necessari comprendre millor
aquest sistema per poder desenvolupar millors estratègies terapèutiques.
Aquesta tesi aborda si les secrecions d’intererohormones induïdes per GSPE modulen la producció de glucagó
pancreàtic i si aquestes secrecions es regulen mitjançant l’estimulació específica de TAS2R que condueix a un control
diferencial de la ingesta d’aliments. Aquesta hipòtesi s’ha avaluat amb estudis in vivo en rates i estudis ex vivo en
mostres intestinals.
Hem identificat que el glucagó és més sensible que la insulina a GSPE, fet que es correlaciona amb una secreció
il·leal de GLP1 millorada.El sistema enteroendocrino se encuentra en el tracto gastrointestinal y controla el apetito y la actividad pancreática endocrina, entre otras funciones. Los compuestos bioactivos que estimulan este sistema son candidatos terapéuticos para tratar patologías relacionadas con estas funciones. Previamente se identificó que un extracto de proantocianidinas de semillas de uva (GSPE) es antidiabético por sus capacidades de mejora de la función de las células y su capacidad saciante, como consecuencia en parte activar del sistema enteroendocrino. Nuestro grupo relacionó las secreciones enteroendocrinas inducidas por polifenoles con la estimulación de receptores del gusto amargo (TAS2R) in vitro, pero si esto se refleja en una ingesta alterada aún se desconoce. Por esto, es necesario comprender mejor este sistema para poder desarrollar mejores estrategias terapéuticas. Esta tesis aborda si las secreciones enteroendocrinas inducidas por GSPE modulan la producción de glucagón pancreático y si estas se regulan mediante la estimulación específica de TAS2R que conduce a un control diferencial de la ingesta. Esta hipótesis se ha evaluado con estudios in vivo en ratas y estudios ex vivo en muestras intestinales. Hemos identificado que el glucagón es más sensible que la insulina a GSPE, lo que se correlaciona con una secreción ileal de GLP1 mejorada.
The enteroendocrine system is located in the gastrointestinal tract and controls appetite and endocrine pancreatic activity, among other functions. Thus, bioactive compounds that stimulate the enteroendocrine system are therapeutic candidates for treating pathologies related to these functions. Previous research has identified a grape-seed proanthocyanidin extract (GSPE) as antidiabetic for its -cell function enhancement abilities and its appetitesuppressing activity at least partly through activating the enteroendocrine system. Moreover, our group has linked the polyphenol-induced enteroendocrine secretions to the stimulation of some bitter taste receptors (TAS2R) in vitro, but whether it results in an altered food intake has not been studied yet. Since little is known of the mechanisms used by polyphenols to stimulate secretory mechanisms of the enteroendocrine system, there is a need to fully comprehend this system to specifically target it with a therapeutic strategy. For this reason, this thesis addressed whether GSPE-induced enterohormone secretions modulate pancreatic glucagon production, and whether these secretions are regulated through the specific stimulation of TAS2R leading to a differential control of food intake. This hypothesis was assessed with in vivo studies in rats and ex vivo studies in intestinal samples.
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Larsen, James D. "Nicotinic Acetylcholine Receptor Dependent Effects of Nicotine on HEK293T and HBO Cells." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5701.
Full textAbstract:
T2R receptors are the classical bitter taste receptors which detect and transduce bitter taste in a subset of taste receptor cells (TRCs). The TRPM5-dependent T2Rs are G-protein coupled receptors (GPCRs) and are linked to G protein, gustducin to initiate an intracellular signaling cascade for the transduction of bitter tastants. Nicotine is bitter. However, at present the transduction mechanisms for the detection of nicotine in are poorly understood. Previous studies from our laboratory using TRPM5 knockout (KO) mice demonstrated that the T2R pathway is insufficient in explaining the taste perception of nicotine. TRPM5 KO mice elicited chorda tympani (CT) taste nerve responses to nicotine, albeit significantly smaller than the wild type (WT) mice and still responded to nicotine as an aversive stimulus. Following addition of mecamylamine (Mec), a non-specific blocker of neuronal nicotinic acetylcholine receptors (nAChRs), CT responses to nicotine were partially inhibited in both WT and TRPM5 KO mice. Mec also decreases the aversive response to nicotine in both WT and TRPM5 KO mice. These studies led to the hypothesis that both a TRPM5-independent and TRPM5-dependent pathways are responsible for the detection and transduction of the bitter taste of nicotine in TRCs. The TRPM5-independent pathway most likely utilizes the nAChRs expressed in TRCs and function as bitter taste receptors for nicotine. We have subsequently demonstrated the expression of nAChRs in a subset of TRPM5-positive TRCs. However, this mechanism is not well understood in other cell types, particularly undifferentiated epithelial cells, such as HEK293T cells. The specific aims of this project were: (i) To identify which components of T2R-dependent taste reception as well as components of nAChRs are expressed in HEK293T cells; (ii) To determine if HEK293T cells co-express these components; (iii) To identify if exposure to nicotine modulates the expression of T2R and nAChR dependent components in HEK293T cells; (iv) To determine if TRCs express functional nAChR ion channels; and (v) To determine if nAChRs are involved in the release of neuropeptides, such as brain-derived neurotrophic factor (BDNF) in HEK293T cells. The data obtained in HEK293T cells was compared with parallel studies on adult cultured human fungiform taste cells (HBO) done independently by Dr. Jie Qian, a postdoctoral fellow in Dr. Vijay Lyall’s lab. The results of combined studies on HBO and HEK293T cells indicates that TRPM5-positive cells also co-express ionotropic nAChRs, comprising a and β subunits. The nAChRs are capable of forming ion pores and when stimulated by nicotine and create a parallel TRPM5-independent pathway for the detection of nicotine. Using molecular and immunocytochemical techniques, our results demonstrate that mRNAs and proteins for bitter taste receptors and downstream intracellular signaling components as well as subunits necessary for the formation of nAChRs are expressed in HBO and HEK293T cells. Results demonstrated that TRPM5-positive HEK293T cells co-expressed nAChR subunits throughout the entire population. Nicotine increased the influx of Ca2+ in a dose dependent manner, which was somewhat reduced by the addition of TRPM5 blocker, triphenylphosphine oxide (TPPO). Both mRNA and protein expression were altered in a biphasic pattern with a maximum increased observed at 0.5 µM nicotine with a decrease in expression at higher concentrations. The synthesis of neurotrophic factor BDNF, required for maturation of taste bud cells and their innervating nerves, increased in HEK293T cells exposed to nicotine, however, nicotine did not trigger the release of BDNF. These results were then compared and contrasted with HBO cells to better understand the comparative effects of nicotine on both undifferentiated and differentiated cells. The data on HBO cells is presented in the Appendix.
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Gous, Andries Gustav Stefanus. "Perceptions and acceptance of grapefruit-like model beverages that vary in taste colour and aroma sensory properties : effects of sensitivity to bitter taste and TAS2R38 and TAS2R19 bitter receptor genes." Thesis, University of Pretoria, 2019. http://hdl.handle.net/2263/77821.
Full textAbstract:
Grapefruit juice is an excellent source of many nutrients and phytochemicals that contribute to a healthy diet. Currently, there is an increasing interest in grapefruit products because consumption appears to be associated with a reduced risk of certain chronic diseases, such as obesity, diabetes, cancers and cardiovascular disease. The consumption of grapefruit (Citrus paradisi Macfadyen) however remains low in South Africa as some individuals like grapefruit and others do not and the reason/s for this variation is not clear. Taste, aroma and colour are important fruit product quality factors that influence consumer preferences. Perception of grapefruit flavour does not depend on only one individual sense, but is the result of multisensory integration of unimodal signals. Where there is a mixture of appearance, taste and aroma signals, cross-modal sensory interaction occurs which may potentially change the intensity and character of flavour perception. Sensory perception is interpreted differently across individuals. The main objective of the study was to determine the effect of varying the bitterness, sweetness, colour and aroma intensities of a grapefruit-like model beverage on the perception of sensory properties and consumer liking of the beverages with the aim of giving guidance to breeders on selection and improvement of grapefruit traits to optimize hedonic value. The second objective of this study was to determine the effects of sensitivity to bitter taste [as determined through 6-propylthiouracil (PROP) taster classification] and genetic
variation in TAS2R38 and TAS2R19 SNP genotypes on hedonic rating of the flavour of grapefruit-like beverages differing in bitter/sweet taste intensity.
A factorial design was used to formulate 36 grapefruit-like beverages with deflavoured clarified apple juice as base and modification of bitter taste (3 levels), sweet taste (3 levels), aroma intensity (2 levels) and colour (red or yellow). Descriptive analysis was used to describe the sensory profiles of the 36 beverages. Hedonic rating of colour, aroma and flavour of the 12 most diverse beverages from the design was measured with a consumer panel. Sensitivity to bitter taste of 96 young African females (18-24 years) was measure and the respondents classified into PROP taster groups. DNA was extracted from the saliva of the participants for genotyping of TAS2R38 and TAS2R19 bitter receptor genes. The subjects also rated the flavour of grapefruit-like beverages differing in bitter taste intensity for hedonic value.
The results showed that varying the bitterness, sweetness, colour and aroma intensity of the grapefruit-like model beverage have an effect on the sensory properties and consumer liking of the beverages. The concentration of naringin in the grapefruit-like beverage increased the bitter taste, aftertaste and grapefruit flavour intensity of the drink. Consumers preferred grapefruit-like beverages with a red colour and low bitterness. Sensitivity to the bitterness of grapefruit beverages and whether there is an association between genetics of bitter taste perception and liking of grapefruit were further explored. The results then showed that respondents’ sensitivity to bitter taste, as well as genetic variation in TAS2R38 and TAS2R19 (single SNP genotypes) are partly responsible for the lower liking of grapefruit model beverages with higher naringin (more bitterness) concentration.
In this study, sensitivity of respondents to bitter taste (PROP status) has been linked to preference for red coloured grapefruit beverages, grapefruit beverages with low bitterness/high sweetness and grapefruit-like beverages with low intensity of grapefruit aroma. This is the first study to report on consumers’ perception and acceptance of grapefruit-like model beverages that vary in taste, colour and aroma sensory properties. People differ genetically in bitter taste sensitivity and this research demonstrated the role of some genetic variables (notably rs10772420 of the TAS2R19 SNP genotype and both rs713598 and rs1726866 of the TAS2R38 SNP genotypes). It is the first study showing the effect of TAS2R38 SNP genotypes on grapefruit liking. It is also the first study to determine the effect of PROP taster status, perception of grapefruit beverage characteristics (e.g. bitterness level, colour type and aroma level) and variation in TAS2R38 and TAS2R19 SNP genotypes on hedonic ratings for colour,
aroma and flavour of grapefruit-like beverages in a group of South African females. So far populations from Africa have been under represented in similar studies. Most studies where a link between rs10772420 and lower bitterness perception and greater liking for unsweetened grapefruit juice was established, included only Caucasians. Studying the role of genetic differences in sensitivity to PROP bitterness (e.g. in taster status) in modulating multisensory grapefruit flavour perception is needed to determine why the liking for grapefruit varies between individuals.
The findings of this study can help researchers and breeders to change properties and traits in grapefruit varieties, can assist product formulators and quality assurance staff to optimize the flavour of grapefruit products for consumer acceptance and to make the generic product more acceptable to a larger portion of the South African population. However, the sample of respondents used in this research represents only a small portion of the South African population and therefore cannot be extrapolated to represent the population. The insights gained from this subgroup may be used to enhance the acceptance of grapefruit products for the larger population.Thesis (PhD)--University of Pretoria, 2019.
Food Science
PhD
Unrestricted
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Loßow, Kristina. "Erzeugung und Charakterisierung von Mausmodellen mit lichtsensitivem Geschmackssystem zur Aufklärung der neuronalen Geschmackskodierung." Phd thesis, Universität Potsdam, 2011. http://opus.kobv.de/ubp/volltexte/2012/5805/.
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Die Wahrnehmung von Geschmacksempfindungen beruht auf dem Zusammenspiel verschiedener Sinneseindrücke wie Schmecken, Riechen und Tasten. Diese Komplexität der gustatorischen Wahrnehmung erschwert die Beantwortung der Frage wie Geschmacksinformationen vom Mund ins Gehirn weitergeleitet, prozessiert und kodiert werden.
Die Analysen zur neuronalen Prozessierung von Geschmacksinformationen erfolgten zumeist mit Bitterstimuli am Mausmodell. Zwar ist bekannt, dass das Genom der Maus für 35 funktionelle Bitterrezeptoren kodiert, jedoch war nur für zwei unter ihnen ein Ligand ermittelt worden. Um eine bessere Grundlage für tierexperimentelle Arbeiten zu schaffen, wurden 16 der 35 Bitterrezeptoren der Maus heterolog in HEK293T-Zellen exprimiert und in Calcium-Imaging-Experimenten funktionell charakterisiert. Die Daten belegen, dass das Funktionsspektrum der Bitterrezeptoren der Maus im Vergleich zum Menschen enger ist und widerlegen damit die Aussage, dass humane und murine orthologe Rezeptoren durch das gleiche Ligandenspektrum angesprochen werden. Die Interpretation von tierexperimentellen Daten und die Übertragbarkeit auf den Menschen werden folglich nicht nur durch die Komplexität des Geschmacks, sondern auch durch Speziesunterschiede verkompliziert.
Die Komplexität des Geschmacks beruht u. a. auf der Tatsache, dass Geschmacksstoffe selten isoliert auftreten und daher eine Vielzahl an Informationen kodiert werden muss. Um solche geschmacksstoffassoziierten Stimuli in der Analyse der gustatorischen Kommunikationsbahnen auszuschließen, sollten Opsine, die durch Licht spezifischer Wellenlänge angeregt werden können, für die selektive Ersetzung von Geschmacksrezeptoren genutzt werden. Um die Funktionalität dieser angestrebten Knockout-Knockin-Modelle zu evaluieren, die eine Kopplung von Opsinen mit dem geschmacksspezifischen G-Protein Gustducin voraussetzte, wurden Oozyten vom Krallenfrosch Xenopus laevis mit dem Zwei-Elektroden-Spannungsklemm-Verfahren hinsichtlich dieser Interaktion analysiert. Der positiven Bewertung dieser Kopplung folgte die Erzeugung von drei Mauslinien, die in der kodierenden Region eines spezifischen Geschmacksrezeptors (Tas1r1, Tas1r2, Tas2r114) Photorezeptoren exprimierten. Durch RT-PCR-, In-situ-Hybridisierungs- und immunhistochemische Experimente konnte der erfolgreiche Knockout der Rezeptorgene und der Knockin der Opsine belegt werden.
Der Nachweis der Funktionalität der Opsine im gustatorischen System wird Gegenstand zukünftiger Analysen sein. Bei erfolgreichem Beleg der Lichtempfindlichkeit von Geschmacksrezeptorzellen dieser Mausmodelle wäre ein System geschaffen, dass es ermöglichen würde, gustatorische neuronale Netzwerke und Hirnareale zu identifizieren, die auf einen reinen geschmacks- und qualitätsspezifischen Stimulus zurückzuführen wären.Taste impression is based on the interaction of taste, smell and touch. To evaluate the nutritious content of food mammals possess five distinct taste qualities: sweet, bitter, umami (taste of amino acids), sour and salty. For bitter, sweet, and umami compounds taste signaling is initiated by binding of tastants to G protein-coupled receptors. The interactions of taste stimuli, usually watersoluble chemicals, with their cognate receptors lead to the activation of the G protein gustducin, which, in turn, initiates a signal resulting in the activation of gustatory afferents. However, details of gustatory signal transmission and processing as well as neural coding are only incompletely understood. This is partly due to the property of some tastants to elicit several sensations simultaneously, unspecific effects caused by the temperature, viscosity, osmolarity, and pH of the solvents, as well as by mechanical stimulation of the tongue during stimulus application. The analysis of gustatory processing of taste information are mainly based on mouse models after stimulation with bitter taste stimuli. Even though it is known that the mouse genome codes for 35 bitter taste receptor genes only few of them had been analysed so far. For better understanding and interpretation of animal experiments 16 mouse bitter receptors had been analysed by Calcium Imaging experiments with HEK293T cells. The data reveal that mouse bitter taste receptors are more narrow tuned than human bitter taste receptors, proving that the ligand spectra of murine and human orthologous receptors are not complient. In order to avoid the disturbing effects of solvents and stimulus application on the analysis of gustatory information transfer and processing, I employ an optogenetical approach to address this problem. For this purpose I generated three strains of gene-targeted mice in which the coding regions of the genes for the umami receptor subunit Tas1r1, the sweet receptor subunit Tas1r2 or the bitter taste receptor Tas2r114 have been replaced by the coding sequences of different opsins (photoreceptors of visual transduction) that are sensitive to light of various wavelengths. In these animals I should be able to activate sweet, bitter, or umami signalling by light avoiding any solvent effects. In initial experiments of this project I demonstrated that the various visual opsins indeed functionally couple to taste signal transduction pathway in oocyte expression system, generating basic knowledge and foundation for the generation of the gene-targeted animals. The knockout-knockin strategies have been successfully realized in the case of all three mouse models, revealed by RT-PCR, in situ hybridization and immunohistochemical analysis of taste papillae. All data confirm that the particular taste receptors have been replaced by the different opsins in taste cells. Further analysis concerning the functional consequences of opsin knockin and taste receptor knockout are part of prospective work.
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Ali, Agha Moutaz. "Physiologie des récepteurs gustatifs chez la mouche de vinaigre (Drosophila melanogaster)." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLA037/document.
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Chez les animaux et en particulier les insectes, l’alimentation comprend une phase d’examen sensoriel qui précède l’ingestion, afin notamment d’éviter d’ingérer des substances toxiques. Cette détection fait intervenir des cellules spécialisées dans la détection de telles molécules, cellules qui sont généralement qualifiées de sensibles aux goûts « amers ». A l’aide d’observations électrophysiologiques et comportementales, nous avons abordé comment un insecte modèle, la drosophile, était capable de détecter des substances potentiellement toxiques mélangées à des sucres à l’aide de ses neurones gustatifs. Dans une première partie, nous avons étudié la détection de la L-canavanine, qui est un acide aminé non protéique. Cette molécule est toxique pour l’homme comme pour les animaux car elle est confondue par le métabolisme avec un acide aminé, la L-arginine, et intégrée à sa place dans les protéines. En utilisant des constructions génétiques et en particulier le système UAS-Gal4, nous avons montré que la Lcanavanine est détectée par des cellules gustatives qui expriment une protéine réceptrice GR66a, qui est impliquée dans la détection de nombreuses substances amères. Nous avons également montré que, contrairement à la caféine, la détection de L-canavanine nécessite des protéines Gαo fonctionnelles. Nous avons ensuite étudié les interactions sucré-amer. Dans un premier travail, nous avons montré que l’addition de Lcanavanine une solution sucrée n’altérait pas la détection des sucres, contrairement à la strychnine qui peut complètement supprimer la détection du sucre dans les cellules gustatives. Grâce à des ablations spécifiques des cellules détectant l’amer, nous avons pu montrer que cette inhibition était une propriété intrinsèque des cellules sensibles aux. sucres. Les cellules sensibles aux sucres auraient donc des sites récepteurs non identifiés, sensibles à certains ligands amers. Nous avons également abordé des interactions inverses, à savoir l’inhibition de la détection de substances amères par des sucres, en confrontant 4 substances amères (denatonium, berberine, caféine, umbelliferone) à 12 sucres. Les observations que nous avons réalisées montrent que certains sucres exercent un effet inhibiteur sur la détection des molécules amères testées. En utilisant des outils génétiques permettant l’ablation des cellules sensibles aux sucres, nous avons montré que cette inhibition est une propriété intrinsèque des cellules sensibles à l’amer. Cependant, cet effet inhibiteur est loin d’être aussi efficace que l’inhibition des substances amères sur la détection des sucres. Dans une dernière partie, nous avons évalué la modulation de la détection gustative à l’aide d’analogues d’une neuro-hormone, la leucokinine, connue pour ses effets sur la diurèse. Lorsqu’elle est mélangée à une solution sucrée, ces analogues inhibent la détection des sucres par les sensilles gustatives, à la fois chez le moustique Aedes aegypti et chez la drosophile. La détection de substances « amères » par les cellules gustatives de drosophiles implique donc deux voies de codage : l’une, spécifique, concerne des cellules dédiées à la détection des substances amères ; l’autre, moins spécifique, affecte les cellules dédiées à la détection des sucres. De manière réciproque, ces cellules dédiées à la détection des molécules sont affectées par la présence de ligands sucrés. Le codage des informations gustatives à la périphérie est donc un phénomène plus complexe qui nécessite d’étudier plus précisément la détection de composés en mélangesIn most animals including insects, ingestion is preceded by a close examination of the food, for example in order to detect the presence of potentially noxious chemicals. This detection involves specialized gustatory cells, which are generally described as sensitive to “bitter” tastes. Using electrophysiology and behavioral observations, we studied how a model insect, Drosophila melanogaster, can detect potentially toxic substances (described here as “bitter”) when mixed with sugar molecules, with their gustatory neurons. In a first part, we studied how L-canavanine is detected. Lcanavanine is a pseudo amino acid, which is confounded with L-arginine by the metabolism. Proteins which include Lcanavanine are non-functional and this compound is toxic for animals including insects. Using genetic constructions based on the UAS-Gal4 expression system, we showed that Lcanavanine is detected by gustatory cells expressing a receptor protein, GR66a, which is specific to most cells capable of detecting bitter substances. We also showed that, contrary to caffeine, the detection of L-canavanine requires functional Gαo proteins. Then, we studied some aspects of the detection of mixtures of sweet and bitter molecules. In a first approach, we contributed to establish that L-canavanine does not impact sugar detection, while other chemicals like strychnine completely inhibit sugar detection. By using the UAS-Gal4 system to ablate bitter-sensitive cells, we could demonstrate that such inhibition is a specific property of sugar- sensitive cells. These cells should have thus receptors for bitter substances which have not been identified yet. We also examined the reverse interaction, which is a possible role of sweet molecules to inhibit the detection of bitter substances. We examined the detection of denatonium, berberine, caffeine and umbelliferone in the presence of 12 different sugars, using behavioral and electrophysiology observations. By using genetic construction to ablate sugar-sensitive cells, we found that the sugar inhibitory action is not due to the presence of sugar-sensitive cells. It should be noted, however that in our experimental conditions, this inhibitory action is less efficient than the inhibition of bitter upon sugar detection. In a last part, we examined the modulation of gustatory perception by analogs of leucokinine, which is a neuropeptide involved in the diuresis of insects. We show that these analogs, when mixed with sugars in solution, can inhibit sugar detection by gustatory sensilla, both in Aedes aegypti mosquitoes and in Drosophila. The detection of bitter molecules by gustatory neurons in Drosophila thus involves two main coding channels: one is specific, and involves gustatory cells dedicated to the detection of bitter molecules; the second one, less specific, is affecting cells which are dedicated to the detection of sugar molecules. Gustatory coding is thus a more complex phenomenon than previously thought on the basis of examining responses to single molecules, thus urging to study the responses of gustatory receptors to more complex and natural mixtures
Book chapters on the topic "Bitter taster receptor"
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Martin, Louis T. P., and Denis J. Dupré. "Bitter Taste Receptors." In Encyclopedia of Signaling Molecules, 553–59. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101498.
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Martin, Louis T. P., and Denis J. Dupré. "Bitter Taste Receptors." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101498-1.
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Shichida, Yoshinori, Takahiro Yamashita, Hiroo Imai, and Takushi Kishida. "Bitter Taste Receptors of Primates." In SpringerBriefs in Biology, 23–34. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54222-3_2.
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Upadhyaya, Jasbir, Nisha Singh, Raj Bhullar, and Prashen Chelikani. "Biochemistry of Human Bitter Taste Receptors." In Bitterness, 1–20. Hoboken, New Jersey: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118590263.ch1.
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Behrens, Maik, and Wolfgang Meyerhof. "Oral and Extraoral Bitter Taste Receptors." In Results and Problems in Cell Differentiation, 87–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14426-4_8.
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Bufe, Bernd, Ellen Schöley-Pohl, Dietmar Krautwurst, Thomas Hofmann, and Wolfgang Meyerhof. "Identification of Human Bitter Taste Receptors." In ACS Symposium Series, 45–59. Washington, DC: American Chemical Society, 2003. http://dx.doi.org/10.1021/bk-2003-0867.ch003.
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Deshpande, Deepak A., and Stephen B. Liggett. "Regulation of Intracellular Calcium by Bitter Taste Receptors on Airway Smooth Muscle." In Calcium Signaling In Airway Smooth Muscle Cells, 409–21. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01312-1_23.
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Naim, M., S. Nir, A. I. Spielman, A. C. Noble, I. Peri, S. Rodin, and M. Samuelov-Zubare. "Hypothesis of Receptor-Dependent and Receptor-Independent Mechanisms for Bitter and Sweet Taste Transduction: Implications for Slow Taste Onset and Lingering Aftertaste." In ACS Symposium Series, 2–17. Washington, DC: American Chemical Society, 2002. http://dx.doi.org/10.1021/bk-2002-0825.ch001.
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Fontanesi, L., F. Bertolini, E. Scotti, G. Schiavo, P. Trevisi, M. Colombo, P. L. Martelli, R. Casadio, and P. Bosi. "Bitter taste receptor genes in pigs: SNP identification by using next- generation semiconductor sequencing." In Energy and protein metabolism and nutrition in sustainable animal production, 297–98. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-781-3_101.
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Shepherd, Gordon M. "Taste Modalities and Wine Tasting." In Neuroenology, 106–14. Columbia University Press, 2016. http://dx.doi.org/10.7312/columbia/9780231177009.003.0012.
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The word “taste” is confusing. Seven meanings of the word are discussed to help clear up the confusion of what it means when applied to wine tasting. The five primary tastes – sweet, salt, sour, bitter, and umami – are explained. Molecular receptors for sweet, bitter and umami have been identified. The organization of the taste bud and their distribution over the tongue and back of the mouth is explained. Movements of the tongue are critical in exposing the taste buds everywhere to the wine + saliva mixture.
Conference papers on the topic "Bitter taster receptor"
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Salvator, H., S. Grassin-Delyle, N. Mantov, C. Abrial, M. Brollo, C. Faisy, E. Naline, L. J. Couderc, and P. Devillier. "Bitter Taste Receptors (TAS2Rs) in Human Lung Macrophages: Receptor Expression and Inhibitory Effects of TAS2R Agonists." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4540.
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Dang, T., A. Lokubandara, N. N. V. Nguyen, P. C. Lai, V. T. Nguyen, and C. Crasto. "User as a bitter tastant: immersive experience within the binding region of a bitter taste receptor." In The 19th International Conference on Modeling & Applied Simulation. CAL-TEK srl, 2020. http://dx.doi.org/10.46354/i3m.2020.mas.019.
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Kuek, L. E., and R. J. Lee. "Expression and Function of Bitter Taste Receptors in the Human Airways." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7478.
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Xu, Wei. "Expansion of a bitter taste receptor family in a polyphagous insect herbivore." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.108651.
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Robinett, Kathryn S., Wayne C. Wang, Molly M. Malone, Demar Pitter, and Stephen B. Liggett. "Agonist-Promoted Desensitization Of Bitter Taste Receptors Expressed On Airway Smooth Muscle." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3643.
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James, Anna, Kameran Daham, Barbro Dahlén, Gunilla Hedlin, Juha Kere, Jon Konradsen, Björn Nordlund, et al. "Expression Of Bitter Taste Receptors On Peripheral Blood Leukocytes From Asthmatic Patients." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6752.
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Pulkkinen, Ville, Jesper Safholm, Martijn Manson, Mikael Adner, and Sven-Erik K. Dahlen. "Further Characterization Of Bitter Taste Receptor Agonists As Bronchodilators In Guinea Pig Trachea." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6477.
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Robinett, Kathryn S., Leann L. Silhan, Deepak A. Deshpande, and Stephen B. Liggett. "Bitter Taste Receptors And β2-Adrenergic Receptors Mediate Relaxation Of Airway Smooth Muscle In An Additive Manner." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6272.
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Gopallawa, I., and R. J. Lee. "Defining the Molecular Mechanisms of Bitter Taste Receptor Activated Nitric Oxide Production in Airway Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1270.
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Dahlén, Sven-Erik, Ville Pulkkinen, Jesper Säfholm, Martijn Manson, and Mikael Adner. "Bitter Taste Receptor Agonists As A Novel Class Of Bronchodilators In Guinea-Pig And Rat Airways." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6381.
Full textReports on the topic "Bitter taster receptor"
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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.
Full textAbstract:
Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.