Cellular and Molecular Mechanisms of Fat Taste Perception

2021 ◽  
Author(s):  
Aziz Hichami ◽  
Amira Sayed Khan ◽  
Naim Akhtar Khan
Keyword(s):  
Molecular Mechanisms ◽  
Taste Perception ◽  
Fat Taste

scholarly journals Mechanism of fat taste perception: Association with diet and obesity

2016 ◽  
Vol 63 ◽  
pp. 41-49 ◽  
Author(s):  
Dongli Liu ◽  
Nicholas Archer ◽  
Konsta Duesing ◽  
Garry Hannan ◽  
Russell Keast
Keyword(s):  
Taste Perception ◽  
Fat Taste

scholarly journals Persistent Epigenetic Reprogramming of Sweet Taste by Diet

2020 ◽  
Author(s):  
Anoumid Vaziri ◽  
Morteza Khabiri ◽  
Brendan T. Genaw ◽  
Christina E. May ◽  
Peter L. Freddolino ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Molecular Mechanisms ◽  
Control Diet ◽  
Sweet Taste ◽  
Taste Perception ◽  
Epigenetic Mechanism ◽  
High Sugar ◽  
Epigenetic Regulator ◽  
Transcriptional Changes ◽  
Gustatory Neurons

AbstractDiets rich in sugar, salt, and fat alter taste perception and food intake, leading to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of D. melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Importantly, half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.

scholarly journals Fatty Acid Lingual Application Activates Gustatory and Reward Brain Circuits in the Mouse

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1246 ◽  
Author(s):  
Yvan Peterschmitt ◽  
Souleymane Abdoul-Azize ◽  
Babar Murtaza ◽  
Marie Barbier ◽  
Amira Khan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Dietary Lipids ◽  
Taste Perception ◽  
Neuronal Activation ◽  
Glut 1 ◽  
Brain Circuits ◽  
Nucleus Of Solitary Tract ◽  
Fat Taste ◽  
Fos Expression ◽  
Reward Pathways

The origin of spontaneous preference for dietary lipids in humans and rodents is debated, though recent compelling evidence has shown the existence of fat taste that might be considered a sixth taste quality. We investigated the implication of gustatory and reward brain circuits, triggered by linoleic acid (LA), a long-chain fatty acid. The LA was applied onto the circumvallate papillae for 30 min in conscious C57BL/6J mice, and neuronal activation was assessed using c-Fos immunohistochemistry. By using real-time reverse transcription polymerase chain reaction (RT-qPCR), we also studied the expression of mRNA encoding brain-derived neurotrophic factor (BDNF), Zif-268, and Glut-1 in some brain areas of these animals. LA induced a significant increase in c-Fos expression in the nucleus of solitary tract (NST), parabrachial nucleus (PBN), and ventroposterior medialis parvocellularis (VPMPC) of the thalamus, which are the regions known to be activated by gustatory signals. LA also triggered c-Fos expression in the central amygdala and ventral tegmental area (VTA), involved in food reward, in conjunction with emotional traits. Interestingly, we noticed a high expression of BDNF, Zif-268, and Glut-1 mRNA in the arcuate nucleus (Arc) and hippocampus (Hipp), where neuronal activation leads to memory formation. Our study demonstrates that oral lipid taste perception might trigger the activation of canonical gustatory and reward pathways.

scholarly journals 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

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1271-1271
Author(s):  
Leta Pilic ◽  
Catherine Anna-Marie Graham ◽  
Nisrin Hares ◽  
Megan Brown ◽  
Jonathan Kean ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Bitter Taste ◽  
Saturated Fat ◽  
Normal Weight ◽  
Taste Perception ◽  
Taste Sensitivity ◽  
Lower Sensitivity ◽  
Fat Intake ◽  
Fat Taste ◽  
Total Fat

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.

scholarly journals Persistent epigenetic reprogramming of sweet taste by diet

2020 ◽  
Vol 6 (46) ◽  
pp. eabc8492
Author(s):  
Anoumid Vaziri ◽  
Morteza Khabiri ◽  
Brendan T. Genaw ◽  
Christina E. May ◽  
Peter L. Freddolino ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Molecular Mechanisms ◽  
Control Diet ◽  
Sweet Taste ◽  
Taste Perception ◽  
Epigenetic Mechanism ◽  
High Sugar ◽  
Epigenetic Regulator ◽  
Transcriptional Changes ◽  
Gustatory Neurons

Diets rich in sugar, salt, and fat alter taste perception and food preference, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of Drosophila melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.

scholarly journals G Protein-Coupled Receptors in Human Fat Taste Perception

2011 ◽  
Vol 37 (2) ◽  
pp. 123-139 ◽  
Author(s):  
M. M. Galindo ◽  
N. Voigt ◽  
J. Stein ◽  
J. van Lengerich ◽  
J.-D. Raguse ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptors ◽  
Taste Perception ◽  
Fat Taste ◽  
G Protein Coupled

scholarly journals Matters of taste: bridging molecular physiology and the humanities

2015 ◽  
Vol 39 (4) ◽  
pp. 288-294 ◽  
Author(s):  
P. K. Rangachari ◽  
Usha Rangachari
Keyword(s):  
Problem Solving ◽  
Molecular Mechanisms ◽  
Cultural Anthropology ◽  
Electronic Tongue ◽  
Problem Based Learning ◽  
Taste Perception ◽  
Nutritional Epidemiology ◽  
Cultural Issues ◽  
Molecular Physiology ◽  
Film Reviews

Taste perception was the focus of an undergraduate course in the health sciences that bridged the sciences and humanities. A problem-based learning approach was used to study the biological issues, whereas the cultural transmutations of these molecular mechanisms were explored using a variety of resources (novels, cookbooks, and films). Multiple evaluation procedures were used: problem summaries and problem-solving exercises (tripartite problem-solving exercise) for the problem-based learning component and group tasks and individual exercises for the cultural issues. Self-selected groups chose specific tasks from a prescribed list of options (setting up a journal in molecular gastronomy, developing an electronic tongue, designing a restaurant for synesthetes, organizing a farmers' market, marketing a culinary tour, framing hedonic scales, exploring changing tastes through works of art or recipe books, and crafting beers for space travel). Individual tasks were selected from a menu of options (book reviews, film reviews, conversations, creative writing, and oral exams). A few guest lecturers (wine making, cultural anthropology, film analysis, and nutritional epidemiology) added more flavor. The course was rated highly for its learning value (8.5 ± 1.2, n = 62) and helped students relate biological mechanisms to cultural issues (9.0 ± 0.9, n = 62).

scholarly journals Effects of oral fat stimulation on fat taste perception and preference among Japanese young men and women

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Yuho Yamauchi ◽  
Mmiko Inoshita ◽  
Kyouko Ueshima ◽  
Yuki Uchida ◽  
Akira Takamata ◽  
...  
Keyword(s):  
Young Men ◽  
Taste Perception ◽  
Men And Women ◽  
Fat Taste

scholarly journals Orosensory Detection of Dietary Fatty Acids Is Altered in CB1R−/− Mice

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1347 ◽  
Author(s):  
Léa Brissard ◽  
Julia Leemput ◽  
Aziz Hichami ◽  
Patricia Passilly-Degrace ◽  
Guillaume Maquart ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endocannabinoid System ◽  
Dietary Fatty Acids ◽  
Taste Perception ◽  
Taste Bud ◽  
Health Issues ◽  
Long Chain Fatty Acid ◽  
Protein Expressions ◽  
Fat Taste ◽  
Taste Bud Cells

Obesity is one of the major public health issues, and its prevalence is steadily increasing all the world over. The endocannabinoid system (ECS) has been shown to be involved in the intake of palatable food via activation of cannabinoid 1 receptor (CB1R). However, the involvement of lingual CB1R in the orosensory perception of dietary fatty acids has never been investigated. In the present study, behavioral tests on CB1R−/− and wild type (WT) mice showed that the invalidation of Cb1r gene was associated with 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 brought about a low preference for dietary fat. No difference in CD36 and GPR120 protein expressions were observed in taste bud cells (TBC) from WT and CB1R−/− mice. However, LCFA induced a higher increase in [Ca2+]i in TBC from WT mice than that in TBC from CB1R−/− mice. TBC from CB1R−/− mice also exhibited decreased Proglucagon and Glp-1r mRNA and a low GLP-1 basal level. We report that CB1R is involved in fat taste perception via calcium signaling and GLP-1 secretion.

scholarly journals Fatty acid sensitivity, intake of high-fat foods, gene polymorphism, and body mass

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Agata Chmurzynska ◽  
Monika Młodzik-Czyżewska ◽  
Anna Malinowska ◽  
Grzegorz Galinski ◽  
Anna Radziejewska ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Body Mass ◽  
Lipid Profiles ◽  
Taste Perception ◽  
Lower Sensitivity ◽  
Fat Intake ◽  
High Fat ◽  
Acid Sensitivity ◽  
Lower Fatty Acid ◽  
Fat Taste

AbstractTaste perception is the main biological determinant of food choice. It has thus been hypothesized that fatty acid sensitivity may affect fat intake. The aim of this study was to examine the relationship between fatty acid sensitivity, frequency of consumption of high-fat products, polymorphism of genes encoding proteins involved in fat taste perception, and body mass.421 people aged 20–40 were enrolled in Poznań, Poland. Body composition was measured using a Bod Pod. The frequency of consumption of high-fat foods was analyzed using an application for mobile devices based on the ecological momentary assessment approach. Food intake was assessed with dietary records. Salad dressings with varying concentrations of canola oil (from 2.5% to 40.0%) were used as stimuli to test fatty acid sensitivity. The individuals were then divided into groups with higher and lower fatty acid sensitivity. Lower sensitivity means that individuals were able to distinguish samples when the oil concentration exceeded 20%. Genotyping of rs1761667 (CD36), rs1573611 (FFAR1), and rs17108973 (FFAR4) was performed using TaqMan probes.57% men and 61% women had higher sensitivity to fatty acids. Higher fatty acid sensitivity was associated with the GG genotype of CD36 (OR = 2.05, p < 0.05). People with different taste sensitivity did not differ in their frequency of consumption of high-fat foods or in their macronutrient intake. There was no association between body mass index (BMI) and fatty acid sensitivity, but people with BMI values below 25 more often ate high-fat products with favorable lipid profiles and less often ate meat high-fat products than subjects with BMI values over 25 (p < 0.001 and p < 0.05, respectively). There was no association between CD36 or FFAR4 genotype and fat intake or frequency of consumption of high-fat foods. People with the minor FFAR1 allele ate sweet high-fat products less often than major allele homozygotes (p < 0.05). Moreover, women ate high-fat products with favorable lipid profiles and sweet and savory high-fat products more frequently than men (p < 0.05, p < 0.001, and p < 0.01), but men ate meat high-fat products more frequently than women (p < 0.01).Concluding, fatty acid sensitivity is associated with polymorphism of the CD36 gene. The frequency of consumption of high-fat foods depends on sex, but not on fatty acid sensitivity, BMI, or CD36 variants.The project was financed by a National Science Centre award (decision number grant no. 2014/15/B/NZ9/02134).

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