Individual Differences Among Children in Sucrose Detection Thresholds: Relationship With Age, Gender, and Bitter Taste Genotype.
Individual Differences Among Children in Sucrose Detection Thresholds: Relationship With Age, Gender, and Bitter Taste Genotype.
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DOI：
10.1097/nnr.0000000000000138
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发表时间：
2016-01
期刊：
影响因子：
2.5
通讯作者：
Mennella JA
中科院分区：
文献类型：
--
作者：
Joseph PV;Reed DR;Mennella JA
很少有研究关注儿童对甜味的敏感性是否存在个体差异，如果存在，这种差异的生物学相关性。我们的目标是了解儿童蔗糖检测阈值的变化与他们的年龄和性别，味觉基因型，身体成分和添加糖的饮食摄入量之间的关系。使用经过验证的、两种选择、强迫选择、配对比较跟踪方法对7至14岁儿童的蔗糖检测阈值进行了单独测试。测试了味觉基因的五种遗传变体：TAS 1 R3和GNAT 3（甜味基因;各一种变体）和苦味受体基因TAS 2 R38（三种变体）。所有儿童都测量了体重和身高。这些儿童中的一个子集被测量了体脂百分比和腰围，并通过24小时饮食回忆提供了额外的糖摄入量。蔗糖阈值范围为0.23至153.8 mM，大多数儿童完成阈值任务（216/235; 92%）。有些孩子是生物学上相关的（即，兄弟姐妹），并且对于遗传分析，研究来自每个家庭的一个兄弟姐妹。苦味基因的变体与蔗糖阈值和糖摄入量有关，但与甜味基因的变体无关;具有两个苦味敏感等位基因的儿童可以在较低浓度下检测到蔗糖（F（2，165）= 4.55，p = 0.01; rs 1726866）并报告食用更多添加糖（% kcal; F（2，62）= 3.64，p = 0.03）。年龄、性别和肥胖指数也与儿童间蔗糖阈值的差异有关;女孩比男孩更敏感（t（214）= 2.0，p = 0.05），年龄较大的儿童比年龄较小的儿童更敏感（r（214）=-0.16，p = 0.02），并且更胖（r（84）=-0.22，p = 0.05）或更多中心性肥胖儿童（r（84）=-0.26，p = 0.02）相对于其他儿童更敏感。苦味敏感性的先天差异可能会影响儿童的膳食糖摄入量，并产生长期的健康后果。在发展中的苦味和甜味系统之间可能存在比以前理解的更复杂的相互作用。
Little research has focused on whether there are individual differences among children in their sensitivity to sweet taste and, if so, the biological correlates of such differences. Our goal was to understand how variations in children’s sucrose detection thresholds relate to their age and gender, taste genotype, body composition, and dietary intake of added sugars. Sucrose detection thresholds in 7- to 14-year-old children were tested individually using a validated, two-alternative, forced-choice, paired-comparison tracking method. Five genetic variants of taste genes were assayed: TAS1R3 and GNAT3 (sweet genes; one variant each) and the bitter receptor gene TAS2R38 (three variants). All children were measured for body weight and height. A subset of these children were measured for the percentage of body fat and waist circumference and provided added sugar intake by 24-hour dietary recall. Sucrose thresholds ranged from 0.23 to 153.8 mM with most of the children completing the threshold task (216/235; 92%). Some children were biologically related (i.e., siblings), and for the genetic analysis, one sibling from each family was studied. Variants in the bitter but not the sweet genes were related to sucrose threshold and sugar intake; children with two bitter-sensitive alleles could detect sucrose at lower concentrations (F(2,165) = 4.55, p = .01; rs1726866) and reported eating more added sugar (% kcal; F(2, 62) = 3.64, p = .03) than did children with less sensitive alleles. Age, gender, and indices of obesity also were related to child-to-child differences in sucrose threshold; girls were more sensitive than boys (t(214) = 2.0, p = .05), older children were more sensitive than younger children (r(214) = −.16, p = .02), and fatter (r(84) = −.22, p = .05) or more centrally obese children (r(84) = −.26, p = .02) were more sensitive relative to others. Inborn differences in bitter sensitivity may affect childhood dietary sugar intake with long-term health consequences. There may be a more complex interplay between the developing bitter and sweet taste systems than previously understood.