甜味的遗传学:感知、进食行为与健康

Harry Stevens, Francesco Piluso, Paolo Gasparini, Y. Mavrommatis, L. Pilic, C. Graham, M. P. Concas
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引用次数: 0

摘要

:背景:甜味部分受遗传影响。味觉受体 1 型成员 2(TAS1R2)中的 rs35874116 单核苷酸多态性(SNP)降低了与 "甜 "分子结合的 G 蛋白偶联受体(GPCR)的可用性。这可能会改变甜味感知、饮食选择和健康结果。然而,这些发现以及与甜味有关的其他基因和通路仍有待确定。因此,我们对 TAS1R2 进行了候选基因研究,并对这些结果进行了全基因组关联研究(GWAS)。研究方法在两个年龄和性别匹配的欧洲队列(英国,n = 50/意大利,n = 235)中调查了 TAS1R2 rs35874116、甜味感知、喜好、饮食和健康。研究采用线性模型来探讨相关性。全球基因组研究是在 2555 名意大利参与者中进行的。研究探讨了与甜食喜好、食物冒险性(FA)、奖赏依赖性(RD)和健康的关联。研究结果TAS1R2的野生型与甜味和食物喜好的增加(p = 0.049,β = 0.62,p = 0.038,β = 0.45)、脂肪消耗的增加(p = 0.006,β = 7.95)和高密度脂蛋白胆固醇的降低(p = 0.025,β = - 3.56)有关。GWAS 在 G 蛋白信号调节器 9(RGS9)基因中发现了 rs58931966。小等位基因与甜食喜好度降低(p = 7.05 × 10 - 9,β = 0.3)、体重指数升高(p = 0.007,β = 0.391)、血糖升高(p = 0.013,β = 1.211)、FA 降低(p = 0.049,β = - 0.065)和 RD 升高(p = 0.011,β = - 3.840)有关。讨论TAS1R2结果表明,味觉受体变异与偏好、饮食和健康相关结果有关。TAS1R2 在 GWAS 中未达到显著性,这表明除了味觉接收外,甜味食物的喜好还受其他途径的影响。RSG9 在纹状体中表达,而纹状体参与了间叶奖赏通路,该通路被甜味激活。RGS9 rs58931966 可能会通过对 G 蛋白信号的负调控来减缓多巴胺能信号对甜味食物的反应。这也许可以解释为什么小等位基因与 RD 减少有关。较低的 FA 可能会降低对苦味蔬菜的偏好,这可以解释较高的 BMI 和血清葡萄糖。FA和RD结果提供了食物选择取决于心理/生物学相互作用的证据。这些结果表明,甜味受多种途径和基因的影响,而这些变化会改变口味、饮食和健康结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Genetics of Sweet Taste: Perception, Feeding Behaviours, and Health
: 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.
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