In the last decade, basic research in chemoreceptor genetics and neurobiology have revolutionized our understanding of individual differences in chemosensation. From an evolutionary perspective, chemosensory variations appear to have arisen in response to different living environments, generally in the avoidance of toxins and to better detect vital food sources. Today, it is often assumed that these differences may drive variable food preferences and choices, with downstream effects on health and wellness. A growing body of evidence indicates chemosensory variation is far more complex than previously believed. However, just because a genetic polymorphism results in altered receptor function in cultured cells or even behavioral phenotypes in the laboratory, this variation may not be sufficient to influence food choice in free living humans. Still, there is ample evidence to indicate allelic variation in TAS2R38 predicts variation in bitterness of synthetic pharmaceuticals (e.g., propylthiouracil) and natural plant compounds (e.g., goitrin), and this variation associates with differential intake of alcohol and vegetables. Further, this is only one of 25 unique bitter taste genes (TAS2Rs) in humans, and emerging evidence suggests other TAS2Rs may also contain polymorphisms that a functional with respect to ingestive behavior. For example, TAS2R16 polymorphisms are linked to the bitterness of naturally occurring plant compounds and alcoholic beverage intake, a TAS2R19 polymorphism predicts differences in quinine bitterness and grapefruit bitterness and liking, and TAS2R31 polymorphisms associate with differential bitterness of plant compounds like aristolochic acid and the sulfonyl amide sweeteners saccharin and acesulfame-K. More critically with respect to food choices, these polymorphisms may vary independently from each other within and across individuals, meaning a monolithic one-size-fits-all approach to bitterness needs to be abandoned. Nor are genetic differences restricted to bitterness. Perceptual variation has also been associated with polymorphisms in genes involved in odors associated with meat defects (boar taint), green/grassy notes, and cilantro, as well as umami and sweet tastes (TAS1R1/2/3). Here, a short primer on receptor genetics is provided, followed by a summary of current knowledge, and implications for human ingestive behavior are discussed.

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化学感应基因的多态性对人类的摄取行为有影响吗？

在过去十年中，化学感受器遗传学和神经生物学的基础研究彻底改变了我们对化学感受器个体差异的理解。从进化的角度来看，化学感应变异似乎是为了响应不同的生活环境而出现的，通常是为了避免毒素和更好地检测重要的食物来源。今天，人们通常认为这些差异可能会导致不同的食物偏好和选择，对健康和健康产生下游影响。越来越多的证据表明化学感应变异比以前认为的要复杂得多。然而，仅仅因为遗传多态性导致培养细胞中受体功能的改变，甚至实验室中的行为表型发生改变，这种变异可能不足以影响自由生活人类的食物选择。仍然，有充分证据表明 TAS2R38 的等位基因变异可预测合成药物（如丙硫氧嘧啶）和天然植物化合物（如甲状腺肿）的苦味变化，这种变化与酒精和蔬菜的不同摄入量有关。此外，这只是人类 25 个独特的苦味基因 (TAS2Rs) 中的一个，新出现的证据表明其他 TAS2Rs 也可能包含对摄取行为有功能的多态性。例如，TAS2R16 多态性与天然植物化合物的苦味和酒精饮料摄入量有关，TAS2R19 多态性预测奎宁苦味和葡萄柚苦味和喜好的差异，TAS2R31 和 TAS2R31 多态性与马兜铃酸和磺酰胺甜味剂糖精和乙酰磺胺酸钾等植物化合物的不同苦味有关。更重要的是，在食物选择方面，这些多态性可能在个体内部和个体之间彼此独立地变化，这意味着需要摒弃单一的一刀切的苦味方法。遗传差异也不限于苦味。感知变异也与肉缺陷（公猪异味）、青/草味、香菜以及鲜味和甜味（TAS1R1/2/3）相关气味相关基因的多态性有关。在这里，提供了受体遗传学的简短入门，然后是当前知识的摘要，并讨论了对人类摄取行为的影响。更重要的是，在食物选择方面，这些多态性可能在个体内部和个体之间彼此独立地变化，这意味着需要放弃单一的一刀切的苦味方法。遗传差异也不限于苦味。感知变异也与肉缺陷（公猪异味）、青/草味、香菜以及鲜味和甜味（TAS1R1/2/3）相关气味相关基因的多态性有关。在这里，提供了受体遗传学的简短入门，然后是当前知识的摘要，并讨论了对人类摄取行为的影响。更重要的是，在食物选择方面，这些多态性可能在个体内部和个体之间彼此独立地变化，这意味着需要放弃单一的一刀切的苦味方法。遗传差异也不限于苦味。感知变异也与肉缺陷（公猪异味）、青/草味、香菜以及鲜味和甜味（TAS1R1/2/3）相关气味相关基因的多态性有关。在这里，提供了受体遗传学的简短入门，然后是当前知识的摘要，并讨论了对人类摄取行为的影响。这意味着需要摒弃单一的一刀切的苦味方法。遗传差异也不限于苦味。感知变异也与肉缺陷（公猪异味）、青/草味、香菜以及鲜味和甜味（TAS1R1/2/3）相关气味相关基因的多态性有关。在这里，提供了受体遗传学的简短入门，然后是当前知识的摘要，并讨论了对人类摄取行为的影响。这意味着需要摒弃单一的、一刀切的苦味方法。遗传差异也不限于苦味。感知变异也与肉缺陷（公猪异味）、青/草味、香菜以及鲜味和甜味（TAS1R1/2/3）相关气味相关基因的多态性有关。在这里，提供了受体遗传学的简短入门，然后是当前知识的摘要，并讨论了对人类摄取行为的影响。