In order to reduce calories in foods and beverages, the food industry routinely uses non-nutritive sweeteners. Unfortunately, many are synthetically derived, and many consumers have a strong preference for natural sweeteners, irrespective of the safety data on synthetic non-nutritive sweeteners. Additionally, many non-nutritive sweeteners elicit aversive side tastes, such as bitter and metallic, in addition to sweetness. Bitterness thresholds of acesulfame-K (AceK) and saccharin are known to vary across bitter taste receptor polymorphisms in TAS2R31. Rebaudioside A (RebA) has been shown to activate hTAS2R4 and hTAS2R14 in vitro. Here, we examined the bitterness and sweetness perception of natural and synthetic non-nutritive sweeteners. In a follow-up to a previous gene association study, participants (n = 122) who had been genotyped previously rated sweet, bitter, and metallic sensations from RebA, rebaudioside D (RebD), aspartame, sucrose, and gentiobiose in duplicate in a single session. For comparison, we also present sweet and bitter ratings of AceK collected in the original experiment for the same participants. At similar sweetness levels, aspartame elicited less bitterness than RebD, which was significantly less bitter than RebA. The bitterness of RebA and RebD showed wide variability across individuals, and bitterness ratings for these compounds were correlated. However, RebA and RebD bitterness did not covary with AceK bitterness. Likewise, single-nucleotide polymorphisms (SNPs) shown previously to explain the variation in the suprathreshold bitterness of AceK (rs3741845 in TAS2R9 and rs10772423 in TAS2R31) did not explain the variation in RebA and RebD bitterness. Because RebA activates hT2R4 and hT2R14, an SNP in TAS2R4 previously associated with variation in bitterness perception was included here; there are no known functional SNPs for TAS2R14. In the present data, a putatively functional SNP (rs2234001) in TAS2R4 did not explain the variation in RebA or RebD bitterness. Collectively, these data indicate that the bitterness of RebA and RebD cannot be predicted by AceK bitterness, reinforcing our view that bitterness is not a simple monolithic trait that is high or low in an individual. This also implies that consumers who reject AceK may not find RebA and RebD aversive, and vice versa. Finally, RebD may be a superior natural non-nutritive sweetener to RebA, as it elicits significantly less bitterness at similar levels of sweetness.

中文翻译：

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莱鲍迪甙 A 和莱鲍迪甙 D 的苦味与 TAS2R9 和 TAS2R31 中的乙酰磺胺酸 K 苦味或多态性没有共变。

为了减少食品和饮料中的卡路里，食品工业通常使用非营养性甜味剂。不幸的是，许多是合成衍生的，并且许多消费者强烈偏爱天然甜味剂，而不管合成非营养甜味剂的安全数据如何。此外，除了甜味之外，许多非营养性甜味剂还会引起令人厌恶的副味，例如苦味和金属味。已知乙酰磺胺酸钾 (AceK) 和糖精的苦味阈值因TAS2R31 中的苦味受体多态性而异。莱鲍迪苷 A (RebA) 已显示在体​​外激活 hTAS2R4 和 hTAS2R14。在这里，我们研究了天然和合成的非营养甜味剂的苦味和甜味。在之前的基因关联研究的后续研究中，参与者（n  = 122) 先前已对来自 RebA、莱鲍迪苷 D (RebD)、阿斯巴甜、蔗糖和龙胆二糖的甜味、苦味和金属感进行了基因分型，并在一次会话中一式两份。为了进行比较，我们还提供了在原始实验中为相同参与者收集的 AceK 的甜味和苦味评级。在相似的甜度水平下，阿斯巴甜引起的苦味比 RebD 少，而 RebD 的苦味明显低于 RebA。RebA 和 RebD 的苦味在个体之间显示出很大的差异，并且这些化合物的苦味等级是相关的。然而，RebA 和 RebD 的苦味与 AceK 的苦味没有共变。同样，之前显示的单核苷酸多态性 (SNP) 可以解释 AceK 阈值上苦味的变化（TAS2R9 中的rs3741845和 TAS2R31 中的rs10772423 ) 不能解释 RebA 和 RebD 苦味的变化。因为使用RebA激活hT2R4和hT2R14，在一个SNP TAS2R4先前与苦味感知变异这里包括相关联; TAS2R14没有已知的功能性 SNP 。在本数据，一个推定的功能性SNP（rs2234001）TAS2R4没有解释 RebA 或 RebD 苦味的变化。总的来说，这些数据表明 RebA 和 RebD 的苦味不能通过 AceK 苦味来预测，强化了我们的观点，即苦味不是一个简单的单一特征，个体的高或低。这也意味着拒绝 AceK 的消费者可能不会发现 RebA 和 RebD 厌恶，反之亦然。最后，RebD 可能是一种优于 RebA 的天然非营养性甜味剂，因为它在类似的甜度水平下引起的苦味明显更少。