一項(xiàng)研究揭示出了奇果的“顛倒味道”的可能機(jī)制,。當(dāng)在舌頭上放幾分鐘之后,，來(lái)自西非的綽號(hào)是“奇果”的紅色莓果的無(wú)味道的奇果蛋白能夠讓檸檬等酸味食物變成楓糖漿那樣甜,。這種效應(yīng)會(huì)在1小時(shí)之內(nèi)逐漸消失,，這在一些科研人員以及有趣的是一些酒吧調(diào)酒員中廣為人知,，調(diào)酒員在所謂的“味覺(jué)顛倒聚會(huì)”上提供這種水果,。Keiko Abe及其同事試圖通過(guò)使用帶有甜味受體（它幫助感受甜味）的人類細(xì)胞的實(shí)驗(yàn)室分析揭開(kāi)奇果蛋白的秘密,。這組作者報(bào)告說(shuō),，當(dāng)預(yù)先用奇果蛋白培養(yǎng)的細(xì)胞接觸到一種酸溶液的時(shí)候，它們受到刺激的程度遠(yuǎn)遠(yuǎn)超過(guò)它們接觸到中性溶液的時(shí)候,。此外,，缺乏這種受體的細(xì)胞不能對(duì)酸做出反應(yīng)，這提示奇果蛋白與這種受體結(jié)合而且在接觸到酸而非中性環(huán)境的時(shí)候不斷激活它,。此外,，在中性環(huán)境下，這種蛋白阻斷了阿斯巴甜和植物甜蛋白等甜味劑的甜味受體的活化,。這組作者使用一個(gè)分子檢驗(yàn)方法追蹤人類味覺(jué)受體hT1R2的究竟哪一部分造成了奇果蛋白的感覺(jué)效應(yīng),。這組作者說(shuō)，這些發(fā)現(xiàn)提示了奇果的味覺(jué)欺騙的一種分子機(jī)制,。(生物谷 Bioon.com)
doi:10.1371/journal.pone.0019448
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Human sweet taste receptor mediates acid-induced sweetness of miraculin
Ayako Koizumi, Asami Tsuchiya, Ken-ichiro Nakajima, Keisuke Ito, Tohru Terada, Akiko Shimizu-Ibuka, Loc Briand, Tomiko Asakura, Takumi Misaka, and Keiko Abe
Miraculin (MCL) is a homodimeric protein isolated from the red berries of Richadella dulcifica. MCL, although flat in taste at neutral pH, has taste-modifying activity to convert sour stimuli to sweetness. Once MCL is held on the tongue, strong sweetness is sensed over 1 h each time we taste a sour solution. Nevertheless, no molecular mechanism underlying the taste-modifying activity has been clarified. In this study, we succeeded in quantitatively evaluating the acid-induced sweetness of MCL using a cell-based assay system and found that MCL activated hT1R2-hT1R3 pH-dependently as the pH decreased from 6.5 to 4.8, and that the receptor activation occurred every time an acid solution was applied. Although MCL per se is sensory-inactive at pH 6.7 or higher, it suppressed the response of hT1R2-hT1R3 to other sweeteners at neutral pH and enhanced the response at weakly acidic pH. Using human/mouse chimeric receptors and molecular modeling, we revealed that the amino-terminal domain of hT1R2 is required for the response to MCL. Our data suggest that MCL binds hT1R2-hT1R3 as an antagonist at neutral pH and functionally changes into an agonist at acidic pH, and we conclude this may cause its taste-modifying activity.
