School of Environmental & Life Sciences, University of Newcastle, PO Box 127, Brush Rd, Ourimbah, NSW, 2258, Australia.
Food Funct. 2011 Aug;2(8):457-65. doi: 10.1039/c1fo10054h. Epub 2011 Jul 18.
Taste perception may influence dietary preferences and nutrient intakes contributing to diet-related disease susceptibility. This study examined bitter taste genetics and whether variation in the TAS2R38 gene at three polymorphic loci (A49P, V262A and I296V) could alter dietary and systemic folate levels and dietary vitamin C intake, and whether a nutrigenetic circuit existed that might link bitter taste, folate/antioxidant status and risk for a colonic adenomatous polyp. TAS2R38 diplotype predicted bitter taste (PROP) phenotype (p value <0.00001) and red cell folate status (p=0.0179) consistent with the diplotype that has the broadest range of bitter perception (AVI/PAV) also possessing the highest average red cell folate value. However, TAS2R38 diplotype did not predict dietary intake of methylfolic acid, pteroylmonoglutamic acid or total folic acid. Neither did it predict dietary intake of vitamin C. Despite this, intake of dietary folate predicts red cell folate with analysis pointing to a key nutrient-nutrient interaction between vitamin C intake and systemic folate status. Analysis of 38 patients with an adenomatous polyp and 164 controls showed that individually, dietary nutrient intake, nutrient status and taste diplotype did not influence polyp risk. However, red cell folate status (in individuals below the population median value) did interact with bitter taste diplotype (AVI/PAV) to predict polyp risk (p=0.0145). Furthermore, synthetic folic acid (below median intake) was statistically associated with adenoma occurrence (p=0.0215); individuals with adenomatous polyps had a 1.77× higher intake than controls. Additionally, stepwise regression taking account of all dietary nutrients showed a tight relationship between methylfolic acid (but not pteroylmonoglutamic acid) intake and red cell folate level in those with a low folate status and occurrence of an adenomatous polyp (p=0.0039). These findings point to a role for folate in the pathoaetiology of adenomatous polyps, with the natural and synthetic vitamers not necessarily having the same biological effect.
味觉感知可能会影响饮食偏好和营养素摄入，从而导致与饮食相关的疾病易感性。本研究探讨了苦味味觉遗传学，以及 TAS2R38 基因在三个多态性位点（A49P、V262A 和 I296V）的变异是否可以改变饮食和系统叶酸水平以及饮食维生素 C 摄入，以及是否存在一个营养遗传回路，将苦味、叶酸/抗氧化剂状态和结直肠腺瘤性息肉的风险联系起来。TAS2R38 二倍型预测苦味（PROP）表型（p 值<0.00001）和红细胞叶酸状态（p=0.0179），与具有最广泛苦味感知范围的二倍型（AVI/PAV）一致，也具有最高的平均红细胞叶酸值。然而，TAS2R38 二倍型并不能预测甲基叶酸、蝶酰谷氨酸或总叶酸的饮食摄入量。它也不能预测维生素 C 的饮食摄入量。尽管如此，饮食叶酸摄入量预测红细胞叶酸，分析指出维生素 C 摄入量和系统叶酸状态之间存在关键的营养素-营养素相互作用。对 38 名腺瘤性息肉患者和 164 名对照者的分析表明，单独的饮食营养素摄入、营养素状态和味觉二倍型并不影响息肉风险。然而，红细胞叶酸状态（在人群中位数以下的个体中）确实与苦味二倍型（AVI/PAV）相互作用，预测息肉风险（p=0.0145）。此外，合成叶酸（摄入量低于中位数）与腺瘤发生有统计学关联（p=0.0215）；患有腺瘤性息肉的个体比对照组的摄入量高 1.77 倍。此外，考虑到所有饮食营养素的逐步回归显示，在叶酸状态低且发生腺瘤性息肉的个体中，甲基叶酸（而非蝶酰谷氨酸）的摄入量与红细胞叶酸水平之间存在紧密关系（p=0.0039）。这些发现表明叶酸在腺瘤性息肉的病理发病机制中起作用，天然和合成维生素不一定具有相同的生物学效应。
