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Natural genetic variation can have a pronounced influence on human taste perception, which in turn may influence food preference and dietary choice. Genome-wide association studies represent a powerful tool to understand this influence. To help optimize the design of future genome-wide-association studies on human taste perception we have used the well-known TAS2R38-PROP association as a tool to determine the relative power and efficiency of different phenotyping and data-analysis strategies. The results show that the choice of both data collection and data processing schemes can have a very substantial impact on the power to detect genotypic variation that affects chemosensory perception. Based on these results we provide practical guidelines for the design of future GWAS studies on chemosensory phenotypes. Moreover, in addition to the TAS2R38 gene past studies have implicated a number of other genetic loci to affect taste sensitivity to PROP and the related bitter compound PTC. None of these other locations showed genome-wide significant associations in our study. To facilitate further, target-gene driven, studies on PROP taste perception we provide the genome-wide list of p-values for all SNPs genotyped in the current study.

Sweet taste perception and preference play crucial roles in dietary habits and health outcomes. Understanding the genetic basis of taste thresholds and preferences can provide insights into individual differences in dietary behavior and susceptibility to metabolic disorders such as type 2 diabetes mellitus (T2DM). In Zambia, there is paucity of data concerning taste perception and preference in relation to genetics among diabetic and non-diabetic individuals. This study aimed to determine the relationship between the genotype and sweet taste thresholds, among individuals with and without T2DM in Zambia. A cross-sectional study was conducted among 89 adults at Livingstone University Teaching Hospital (42 non-diabetic and 47 diabetics). Saliva samples were used to determine the TRPV1 rs4790522, and TAS1R3 rs307355 genotype. We assessed sweet taste threshold and preference using a series of aqueous sucrose solutions. Demographic characteristics, anthropometrics, lifestyle factors, and dietary habits were collected using a structured questionnaire. Sweet taste threshold positively correlated with preferred concentration in both groups (p < 0.05). A higher proportion of PwT2D with elevated preferred sweet concentrations carried one or both homozygous risk alleles (77.8%, TT/AA). When compared to healthy controls, PwT2D had higher BMI, systolic and diastolic blood pressure, and pulse rate. They also exhibited higher taste thresholds but lower preferred concentrations, though this group was significantly older, potentially confounding results. These findings suggest taste perception and genetic variation may differ in PwT2D, highlighting the need for further research in Sub-Saharan African populations to inform personalized, cost-effective treatment strategies. However, studies with a larger sample size are required to validate our findings.

Taste sensitivity to PROP varies greatly among individuals and is associated with polymorphisms in the bitter receptor gene TAS2R38, and with differences in fungiform papilla density on the anterior tongue surface. Recently we showed that the PROP non-taster phenotype is strongly associated with the G variant of polymorphism rs2274333 (A/G) of the gene that controls the salivary trophic factor, gustin. The aims of this study were 1) to investigate the role of gustin gene polymorphism rs2274333 (A/G), in PROP sensitivity and fungiform papilla density and morphology, and 2) to investigate the effect of this gustin gene polymorphism on cell proliferation and metabolic activity. Sixty-four subjects were genotyped for both genes by PCR techniques, their PROP sensitivity was assessed by scaling and threshold methods, and their fungiform papilla density, diameter and morphology were determined. In vitro experiments examined cell proliferation and metabolic activity, following treatment with saliva of individuals with and without the gustin gene mutation, and with isolated protein, in the two iso-forms. Gustin and TAS2R38 genotypes were associated with PROP threshold (p=0.0001 and p=0.0042), but bitterness intensity was mostly determined by TAS2R38 genotypes (p<0.000001). Fungiform papillae densities were associated with both genotypes (p<0.014) (with a stronger effect for gustin; p=0.0006), but papilla morphology was a function of gustin alone (p<0.0012). Treatment of isolated cells with saliva from individuals with the AA form of gustin or direct application of the active iso-form of gustin protein increased cell proliferation and metabolic activity (p<0.0135). These novel findings suggest that the rs2274333 polymorphism of the gustin gene affects PROP sensitivity by acting on fungiform papilla development and maintenance, and could provide the first mechanistic explanation for why PROP super-tasters are more responsive to a broad range of oral stimuli.

Individual taste sensitivity influences food preferences, nutritional control, and health, and differs greatly between individuals. The purpose of this study was to establish a method of measuring and quantifying an individual’s taste sensitivity and to evaluate the relationship between taste variation and genetic polymorphisms in humans using agonist specificities of the bitter taste receptor gene, TAS2R38, with the bitter compound 6-n-propylthiouracil (PROP). We precisely detected the threshold of PROP bitter perception by conducting the modified two-alternative forced-choice (2AFC) procedure with the Bayesian staircase procedure of the QUEST method and examined genetic variation in TAS2R38 in a Japanese population. There were significant differences in PROP threshold between the three TAS2R38 genotype pairs for 79 subjects: PAV/PAV vs AVI/AVI, p < 0.001; PAV/AVI vs AVI/AVI, p < 0.001; and PAV/PAV vs PAV/AVI, p < 0.01. Our results quantified individual bitter perception as QUEST threshold values: the PROP bitter perception of individuals with the PAV/PAV or PAV/AVI genotypes was tens to fifty times more sensitive than that of an individual with the AVI/AVI genotype. Our analyses provide a basic model for the accurate estimation of taste thresholds using the modified 2AFC with the QUEST approach.

Bitterness from phenylthiocarbamide and 6-n-propylthiouracil (PROP) varies with polymorphisms in the TAS2R38 gene. Three SNPs form two common (AVI, PAV) and four rare haplotypes (AAI, AAV, PVI, and PAI). AVI homozygotes exhibit higher detection thresholds and lower suprathreshold bitterness for PROP compared to PAV homozygotes and heterozygotes, and these differences may influence alcohol and vegetable intake. Within a diplotype, substantial variation in suprathreshold bitterness persists, and some AVI homozygotes report moderate bitterness at high concentrations. A second receptor encoded by a gene containing a functional polymorphism may explain this. Early work has suggested that PROP might activate TAS2R4 in vitro, but later work did not replicate this. Here, we identify three TAS2R4 SNPs that result in three diplotypes—SLN/SLN, FVS/SLN, and FVS/FVS—which make up 25.1%, 44.9%, and 23.9% of our sample. These TAS2R4 haplotypes show minimal linkage disequilibrium with TAS2R38, so we examined the suprathreshold bitterness as a function of both. The participants (n = 243) rated five PROP concentrations in duplicate, interleaved with other stimuli. As expected, the TAS2R38 haplotypes explained ~29% (p < 0.0001) of the variation in the bitterness ratings, with substantial variation within the haplotypes (AVI/AVI, PAV/AVI, and PAV/PAV). Notably, the TAS2R4 diplotypes (independent of the TAS2R38 haplotypes) explained ~7–8% of the variation in the bitterness ratings (p = 0.0001). Given this, we revisited if PROP could activate heterologously expressed TAS2R4 in HEK293T cells, and calcium imaging indicated 3 mM PROP is a weak TAS2R4 agonist. In sum, our data are consistent with the second receptor hypothesis and may explain the recovery of the PROP tasting phenotype in some AVI homozygotes; further, this finding may potentially help explain the conflicting results on the TAS2R38 diplotype and food intake.

In Drosophila, detection of tastants is thought to be mediated by members of a family of 68 gustatory receptors (Grs). However, only one receptor, Gr5a, has been associated with a sugar, and it appears to be activated specifically by trehalose. It is unclear whether other sugar receptors are activated by single or multiple sugars. Currently, no Grs are known to colocalize with Gr5a. Such Grs would be candidate sugar receptors because Gr5a-expressing cells function in the responses to attractive tastants. Here we use an \"mRNA tagging\" approach to identify Gr RNAs that are coexpressed with Gr5a. We found that all seven Grs most related to Gr5a (Gr64a-f and Gr61a) were expressed in Gr5a-expressing cells, whereas none of the other Grs examined were enriched in these Gr neurons (GRNs). We characterized the role of one Gr5a-related receptor, Gr64a, and found that it was required for the behavioral responses to glucose, sucrose, and maltose. Gr64a was required for GRN function because action potentials induced by these sugars were dependent on expression of Gr64a in GRNs. These data demonstrate that multiple Grs are coexpressed with Gr5a and that Drosophila Gr64a is required for the responses to multiple sugars.

Salty taste perception affects salt intake, of which excess amounts is a major public health concern. Gene polymorphisms in salty taste receptors, zinc status and their interaction may affect salty taste perception. In this study, we examined the relationships among the α-epithelial sodium channel (αENaC) A663T genotype, zinc intake, and salty taste perception including salty taste acuity and preference in healthy young adults. The αENaC A663T genotype was determined by the PCR-restriction fragment length polymorphism in 207 adults. Zinc intake was examined by one 24-h recall and a two-day dietary record. Salty taste acuity and preference were determined by measuring the salty taste recognition threshold and the preferred salinity of beansprout soup, respectively. Men had significantly higher thresholds and preferences for salty taste than women did (p < 0.05). In women, the salty taste threshold was significantly lower in the highest tertile of available zinc intake than in the lowest tertile (12.2 mM and 17.6 mM, respectively, p = 0.02). Interestingly, a significant inverse association between available zinc intake and salty taste threshold was found only in women with αENaC AA homozygotes (β = −0.833, p = 0.02), and no such association was found in T663 allele carriers. The salty taste preference was not associated with the αENaC A663T genotype or available zinc intake in either sex. In conclusion, our data suggest that gene-nutrient interactions between the αENaC A663T genotype and available zinc intake play a role in determining the salty taste acuity in young women.

Introduction: Dental caries is one of the most prevalent infectious diseases to affl ict humanity. Although caries has multifactorial etiology, inherited genetic behavior and taste threshold may play an important role on caries. Material and Method: Thirty mothers and thirty children in the age group of 6-14 years of both sexes who have stable mental condition and ASA physical status were selected for the study & 6-n-propylthiouracil testing is done. Results: It is observed that nontaster siblings have higher caries prevalence than medium tasters and supertasters. Discussion: Genetic sensitivity to taste is an inherited trait in children from their parents, inheritance from mother being more pronounced. Hence, this study is intended. Conclusion: Dental caries is multi-factorial. No significant correlation between susceptibility of mother and child to genetic sensitivity exists, and genetic sensitivity is not the only criteria for severity.

The genetic basis of androstenone anosmia has been well studied due to androstenone's putative role as a human sex pheromone and its presence in pork meat. Polymorphisms have been identified on the olfactory receptor gene OR7D4, which significantly affect perception of androstenone pleasantness and intensity in several Western populations. This study aims to investigate androstenone sensitivity and the influence of OR7D4 polymorphisms in non-Western populations. Androstenone perception was tested in 132 individuals from Madagascar using a double three-alternative choice test with two concentrations of androstenone (0.17 and 1.7 µg/ml). We found that Malagasy populations described this molecule in a similar way to European populations, and 21% of the sample was not able to smell androstenone. In contrast to previous studies, there was no significant evidence of the influence of rs61729907: C>T (R88W) and rs5020278: C>T polymorphisms (T133M) on androstenone sensitivity in Malagasy populations. We found, however, a significant effect of the polymorphism rs61732668 (P79L) and a significant difference in androstenone perception between populations in different locations across Madagascar. This study indicates the existence of population-specific factors in androstenone sensitivity, suggesting that population history has a role in shaping an individual's smell and flavor preferences and food preferences in general.

This study is the first attempt to link quantified phenylthiocarbamide bitter taste recognition threshold with susceptibility to motion sickness. The study was conducted on a sample of 291 teenage Rajput children (146 males and 145 females; age range 13-19 years) from the Sirmour district of Himachal Pradesh, India. Phenylthiocarbamide taste sensitivity was measured by administering a serial dilution of a freshly prepared phenylthiocarbamide solution, following the method of Harris and Kalmus. Motion sickness susceptibility was assessed retrospectively via interview. About 40 per cent of the subjects had experienced motion sickness in the past. The mean and standard deviation of phenylthiocarbamide taste thresholds in non-tasters and tasters were 0.83 +/- 0.87 and 7.98 +/- 1.86, respectively. A bimodal distribution test (D/S) index of 5.24 confirmed bimodality of phenylthiocarbamide taste threshold distribution. The Mann-Whitney U test rejected the null hypothesis of mu 1 = mu 2 and thus confirmed the existence of differences in the distributions of phenylthiocarbamide taste threshold between individuals susceptible and not susceptible to motion sickness. Individuals susceptible to motion sickness had lower mean and median taste thresholds, indicating higher phenylthiocarbamide taste sensitivity, compared with non-susceptible individuals. The frequency of non-tasters was about 10 per cent in both motion sickness susceptible and non-susceptible individuals. The simple division of phenylthiocarbamide tasting ability into tasters and non-tasters was a less sensitive criterion with which to measure the association of this ability with motion sickness susceptibility. However, further differentiation of tasters into weak threshold, medium threshold and super threshold ('supersensitive') tasters clearly revealed a highly significantly increased risk of motion sickness in super threshold tasters (i.e. threshold solution number >or=12). The ratio of motion sickness susceptible individuals to non-susceptible individuals was 1:1.7 for non-tasters (threshold solution numbers zero to three) and weak and medium tasters (threshold solution numbers four to 11), but the trend was reversed for super threshold tasters (threshold solution numbers 12 and 13), in whom the ratio was 2:1. Individuals exhibiting greater phenylthiocarbamide taste acuity (i.e. supersensitive tasters) had a higher susceptibility to motion sickness than did non-, weak and medium phenylthiocarbamide tasters, as measured in terms of their taste thresholds (i.e. threshold solution numbers zero to 11).