Harry Stevens, Francesco Piluso, Paolo Gasparini, Y. Mavrommatis, L. Pilic, C. Graham, M. P. Concas
{"title":"The Genetics of Sweet Taste: Perception, Feeding Behaviours, and Health","authors":"Harry Stevens, Francesco Piluso, Paolo Gasparini, Y. Mavrommatis, L. Pilic, C. Graham, M. P. Concas","doi":"10.3390/proceedings2023091342","DOIUrl":null,"url":null,"abstract":": Background: Sweet taste is partly modified by genetics. The rs35874116 single-nucleotide polymorphism (SNP) in taste receptor type 1 member 2 (TAS1R2) reduces the availability of a G protein-coupled receptor (GPCR), which binds to ‘sweet’ molecules. This might alter sweet taste perception, diet choices, and health outcomes. However, these findings, and other genes and pathways involved in sweet taste are yet to be identified. Therefore, a candidate gene study on TAS1R2 and a genome-wide association study (GWAS) exploring these outcomes were performed. Methods: TAS1R2 rs35874116, sweet perception, liking, diet, and health were investigated in two age-and sex-matched European cohorts (UK, n = 50/Italy, n = 235). Linear models were used to explore associations. The GWAS was performed with 2555 Italian participants. Associations with sweet food liking, food adventurousness (FA), reward dependence (RD), and health were explored. Results: The wildtype of TAS1R2 was associated with increased sweet taste and food liking ( p = 0.049, β = 0.62, p = 0.038, β = 0.45), increased fibre consumption ( p = 0.006, β = 7.95), and decreased HDL cholesterol ( p = 0.025, β = − 3.56). The GWAS identified rs58931966 in the regulator of G-protein signalling 9 (RGS9) gene. The minor allele was associated with decreased sweet food liking ( p = 7.05 × 10 – 9, β = 0.3), a higher BMI ( p = 0.007, β = 0.391), serum glucose ( p = 0.013, β = 1.211), lower FA ( p = 0.049, β = − 0.065), and RD ( p = 0.011, β = − 3.840). Discussion: The TAS1R2 results show that taste receptor variations are associated with preference, diet, and health-related outcomes. TAS1R2 not reaching significance in the GWAS shows that sweet food liking is modified by pathways besides taste reception. RSG9 is expressed in the striatum, which is involved in the mesolimbic reward pathway, which is activated by sweet taste. RGS9 rs58931966 may moderate dopaminergic signalling in response to sweet foods via the negative regulation of G-protein signalling. This might explain why the minor allele was associated with reduced RD. The lower FA might decrease preference for bitter-tasting vegetables, which could explain the higher BMI and serum glucose. The FA and RD results provide evidence that food choice depends on psychological/biological interplay. These results show that sweet taste is modified by multiple pathways and genes, and variations can modify taste, diet, and health outcomes.","PeriodicalId":507355,"journal":{"name":"The 14th European Nutrition Conference FENS 2023","volume":"25 22","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The 14th European Nutrition Conference FENS 2023","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/proceedings2023091342","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
: Background: Sweet taste is partly modified by genetics. The rs35874116 single-nucleotide polymorphism (SNP) in taste receptor type 1 member 2 (TAS1R2) reduces the availability of a G protein-coupled receptor (GPCR), which binds to ‘sweet’ molecules. This might alter sweet taste perception, diet choices, and health outcomes. However, these findings, and other genes and pathways involved in sweet taste are yet to be identified. Therefore, a candidate gene study on TAS1R2 and a genome-wide association study (GWAS) exploring these outcomes were performed. Methods: TAS1R2 rs35874116, sweet perception, liking, diet, and health were investigated in two age-and sex-matched European cohorts (UK, n = 50/Italy, n = 235). Linear models were used to explore associations. The GWAS was performed with 2555 Italian participants. Associations with sweet food liking, food adventurousness (FA), reward dependence (RD), and health were explored. Results: The wildtype of TAS1R2 was associated with increased sweet taste and food liking ( p = 0.049, β = 0.62, p = 0.038, β = 0.45), increased fibre consumption ( p = 0.006, β = 7.95), and decreased HDL cholesterol ( p = 0.025, β = − 3.56). The GWAS identified rs58931966 in the regulator of G-protein signalling 9 (RGS9) gene. The minor allele was associated with decreased sweet food liking ( p = 7.05 × 10 – 9, β = 0.3), a higher BMI ( p = 0.007, β = 0.391), serum glucose ( p = 0.013, β = 1.211), lower FA ( p = 0.049, β = − 0.065), and RD ( p = 0.011, β = − 3.840). Discussion: The TAS1R2 results show that taste receptor variations are associated with preference, diet, and health-related outcomes. TAS1R2 not reaching significance in the GWAS shows that sweet food liking is modified by pathways besides taste reception. RSG9 is expressed in the striatum, which is involved in the mesolimbic reward pathway, which is activated by sweet taste. RGS9 rs58931966 may moderate dopaminergic signalling in response to sweet foods via the negative regulation of G-protein signalling. This might explain why the minor allele was associated with reduced RD. The lower FA might decrease preference for bitter-tasting vegetables, which could explain the higher BMI and serum glucose. The FA and RD results provide evidence that food choice depends on psychological/biological interplay. These results show that sweet taste is modified by multiple pathways and genes, and variations can modify taste, diet, and health outcomes.