法國(guó)國(guó)家健康與醫(yī)學(xué)研究所２７日宣布，該研究所日前發(fā)現(xiàn)了人體內(nèi)維生素Ｃ的輸送機(jī)制，該機(jī)制能夠幫助人體有效地?cái)z取食物中的維生素Ｃ，維持身體健康。
據(jù)該研究所介紹，維生素Ｃ是人體內(nèi)眾多生理過程的重要參與者。如果人缺乏維生素Ｃ，就會(huì)患上敗血癥等疾病。在自然界，絕大多數(shù)的哺乳動(dòng)物都能在體內(nèi)自行合成維生素Ｃ，但奇怪的是，包括人類在內(nèi)的一部分靈長(zhǎng)類動(dòng)物卻不具備這種能力。有專家推測(cè)，這種能力的缺失源自于４０００萬(wàn)年前的基因突變。
法國(guó)國(guó)家健康與醫(yī)學(xué)研究所的納奧米·泰勒和她的科研小組通過研究發(fā)現(xiàn)，在人體內(nèi)，維生素Ｃ氧化物的“運(yùn)輸”是由一種名為Ｇｌｕｔ１的蛋白質(zhì)來完成的，Ｇｌｕｔ１又稱葡萄糖轉(zhuǎn)運(yùn)蛋白，是細(xì)胞運(yùn)輸葡萄糖的重要載體。
泰勒發(fā)現(xiàn)，Ｇｌｕｔ１蛋白只出現(xiàn)在不具備維生素Ｃ合成能力的生物的血細(xì)胞里。有趣的是，一身二職的Ｇｌｕｔ１蛋白在運(yùn)輸過程中，會(huì)對(duì)維生素Ｃ給予“優(yōu)先”的待遇，然后才去運(yùn)送葡萄糖。正是這種蛋白質(zhì)的存在，維生素Ｃ的氧化物才能迅速被血細(xì)胞吸收，然后轉(zhuǎn)化為新的形式，方便人體吸收。
研究人員認(rèn)為，在約４０００萬(wàn)年前的基因突變之后，人體內(nèi)才逐漸形成了這套補(bǔ)償機(jī)制，以保證維生素Ｃ的足量攝入。目前該研究成果已經(jīng)發(fā)表在一期的美國(guó)《細(xì)胞》雜志上。
Erythrocyte Glut1 Triggers DehydroASCorbic Acid Uptake in Mammals Unable to Synthesize Vitamin C
Amélie Mon-Hagen,1 Sandrina Kinet,1 Nicolas Manel,1,4 Cédric Mongellaz,1 Rainer Prohaska,2 Jean-Luc Battini,1 Jean Delaunay,3 Marc Sitbon,1 and Naomi Taylor1,Cell發(fā)現(xiàn)人體內(nèi)維生素Ｃ的輸送機(jī)制
1 Institut de Génétique Moléculaire de Montpellier, CNRS, Université Montpellier I and II, Montpellier, France
2 Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, Vienna Biocenter, Vienna A-1030, Austria
3 Hématologie, Hôpital de Bicêtre, APHP, INSERM U779, Faculté de Médecine Paris-Sud, Le Kremlin-Bicêtre, France
Summary
Of all cells, human erythrocytes express the highest level of the Glut1 glucose transporter. However, the regulation and function of Glut1 during erythropoiesis are not known. Here, we report that glucose transport actually decreases during human erythropoiesis despite a >3-log increase in Glut1 transcripts. In contrast, Glut1-mediated transport of L-dehydroascorbic acid (DHA), an oxidized form of ascorbic acid (AA), is dramatically enhanced. We identified stomatin, an integral erythrocyte membrane protein, as regulating the switch from glucose to DHA transport. Notably though, we found that erythrocyte Glut1 and associated DHA uptake are unique traits of humans and the few other mammals that have lost the ability to synthesize AA from glucose. Accordingly, we show that mice, a species capable of synthesizing AA, express Glut4 but not Glut1 in mature erythrocytes. Thus, erythrocyte-specific coexpression of Glut1 with stomatin constitutes a compensatory mechanism in mammals that are unable to synthesize vitamin C.