Kuhn Christina, Bufe Bernd, Winnig Marcel, Hofmann Thomas, Frank Oliver, Behrens Maik, Lewtschenko Tatjana, Slack Jay P, Ward Cynthia D, Meyerhof Wolfgang
German Institute of Human Nutrition Potsdam-Rehbruecke, Department of Molecular Genetics, 14558 Nuthetal, Germany.
J Neurosci. 2004 Nov 10;24(45):10260-5. doi: 10.1523/JNEUROSCI.1225-04.2004.
Weight-conscious subjects and diabetics use the sulfonyl amide sweeteners saccharin and acesulfame K to reduce their calorie and sugar intake. However, the intrinsic bitter aftertaste, which is caused by unknown mechanisms, limits the use of these sweeteners. Here, we show by functional expression experiments in human embryonic kidney cells that saccharin and acesulfame K activate two members of the human TAS2R family (hTAS2R43 and hTAS2R44) at concentrations known to stimulate bitter taste. These receptors are expressed in tongue taste papillae. Moreover, the sweet inhibitor lactisole did not block the responses of cells transfected with TAS2R43 and TAS2R44, whereas it did block the response of cells expressing the sweet taste receptor heteromer hTAS1R2-hTAS1R3. The two receptors were also activated by nanomolar concentrations of aristolochic acid, a purely bitter-tasting compound. Thus, hTAS2R43 and hTAS2R44 function as cognate bitter taste receptors and do not contribute to the sweet taste of saccharin and acesulfame K. Consistent with the in vitro data, cross-adaptation studies in human subjects also support the existence of common receptors for both sulfonyl amide sweeteners.
关注体重的人群和糖尿病患者使用磺酰胺类甜味剂糖精和乙酰磺胺酸钾来减少热量和糖分摄入。然而，由未知机制引起的内在苦味余味限制了这些甜味剂的使用。在此，我们通过在人胚肾细胞中的功能表达实验表明，糖精和乙酰磺胺酸钾在已知能刺激苦味的浓度下激活了人类TAS2R家族的两个成员（hTAS2R43和hTAS2R44）。这些受体在舌乳头中表达。此外，甜味抑制剂乳糖唑并未阻断用TAS2R43和TAS2R44转染的细胞的反应，而它确实阻断了表达甜味受体异源二聚体hTAS1R2 - hTAS1R3的细胞的反应。这两种受体也被纳摩尔浓度的马兜铃酸激活，马兜铃酸是一种纯苦味化合物。因此，hTAS2R43和hTAS2R44作为同源苦味受体发挥作用，对糖精和乙酰磺胺酸钾的甜味没有贡献。与体外数据一致，在人类受试者中的交叉适应研究也支持磺酰胺类甜味剂存在共同受体。
