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Abstract
Orosensory intensity, including intensity of a taste sensation, varies greatly among individuals for an array of taste stimuli'. Taste intensity perception is influenced by taste genetics 2-4 as well as other environmental factors such as ear infections or oral infections that can cause taste dysfunction. Variation in taste intensity, either through normal genetic variation or environmental factors, have been shown to explain differences in liking, and in some cases, consumption of foods that may influence long term health outcomes and chronic disease risk, such as high-fat foods-10, sweets, salt", alcohol 12-16, and vegetables 17.38. In addition, taste variation also explains individual differences in important health markers, such as adiposity 6,19,20,21 serum lipids 22-23, and blood pressure".
This thesis follows the conceptual model shown in Figure 1. Chapter II. examines taste phenotype and its novel associations with an intronic SNP in TASIRI, one of the genes responsible for the taste of umami (savory). Chapter III develops the protocol to measure taste phenotype in population-based studies, by integrating our current laboratory-based understanding of tests that capture variability in taste intensity perception and by using intensity markers that are important for predicting health outcomes.
Some variation in taste and oral sensation relates to polymorphisms in genes that encode for taste receptors. Since little is known about the contributions of TASIRI variation to functional differences in taste perception, we tested associations between aTASIR/ intronic SNP (rs17492553, T) and preferences for dietary sources of glutamate as well as variability in oral sensory intensity. Given known associations of TAS2R38 haplotypes (a bitter taste receptor) with the bitterness of propylthiouracil (PROP) 2, a phenotypic marker for supertasting (heightened taste sensations across all intensities), and preference for bitter vegetables" and alcohol", we hypothesized that rs17492553, an intronic SNP putatively associated with genetranslation, may also be a potential marker of overall variability in orosensory intensity, and influence preferences for dietary sources of glutamate. The study details and results are described in Chapter II.
Chapter III describes our involvement, as part of the Taste Panel of NIH Toolbox initiative, in proposing a standard set of taste measures for use in population- based assessment of taste function. Taste measures had to meet the Toolbox criteria of being minimally burdensome to subjects and investigators, cover the full range of taste function (not just taste dysfunction) and be relevant to health outcomes. By participating in a taste team and collaborating with other taste experts across the nation, we thoroughly evaluated existing laboratory procedures for assessing taste function and phenotype for inclusion in the Toolbox kit. After a considerable discussion, we proposed to assess taste function by scaling of the taste intensity oftwo bitter probes-one to test regionally on the tongue tip and through whole mouthtasting, and the other as a taste gene phenotype. In a counter-balanced design with asample of 100 healthy adults (18-30 yrs, 59 F), we compared the Toolbox measures totaste measures commonly used in laboratory studies. Our study design and results aredescribed in Chapter III.
