人体内维生素Ｃ的输送机制资讯

法国国家健康与医学研究所２７日宣布，该研究所日前发现了人体内维生素Ｃ的输送机制，该机制能够帮助人体有效地摄取食物中的维生素Ｃ，维持身体健康。
据该研究所介绍，维生素Ｃ是人体内众多生理过程的重要参与者。如果人缺乏维生素Ｃ，就会患上败血症等疾病。在自然界，绝大多数的哺乳动物都能在体内自行合成维生素Ｃ，但奇怪的是，包括人类在内的一部分灵长类动物却不具备这种能力。有专家推测，这种能力的缺失源自于４０００万年前的基因突变。
法国国家健康与医学研究所的纳奥米·泰勒和她的科研小组通过研究发现，在人体内，维生素Ｃ氧化物的“运输”是由一种名为Ｇｌｕｔ１的蛋白质来完成的，Ｇｌｕｔ１又称葡萄糖转运蛋白，是细胞运输葡萄糖的重要载体。
泰勒发现，Ｇｌｕｔ１蛋白只出现在不具备维生素Ｃ合成能力的生物的血细胞里。有趣的是，一身二职的Ｇｌｕｔ１蛋白在运输过程中，会对维生素Ｃ给予“优先”的待遇，然后才去运送葡萄糖。正是这种蛋白质的存在，维生素Ｃ的氧化物才能迅速被血细胞吸收，然后转化为新的形式，方便人体吸收。
研究人员认为，在约４０００万年前的基因突变之后，人体内才逐渐形成了这套补偿机制，以保证维生素Ｃ的足量摄入。目前该研究成果已经发表在一期的美国《细胞》杂志上。
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发现人体内维生素Ｃ的输送机制
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.