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婴儿的微量元素营养——分子方法

Trace element nutrition of infants--molecular approaches.

作者信息

Lönnerdal Bo

机构信息

Department of Nutrition, University of California, One Shields Avenue, Davis, CA 95616, USA.

出版信息

J Trace Elem Med Biol. 2005;19(1):3-6. doi: 10.1016/j.jtemb.2005.03.004.

DOI:10.1016/j.jtemb.2005.03.004
PMID:16240664
Abstract

Newborn infants are exposed to widely varying intakes of trace elements, but little is known about their ability to homeostatically adjust to these intakes. Recent discoveries of several metal ion transporters in the small intestine are likely to enhance our understanding of molecular mechanisms regulating trace element absorption. Iron absorption is regulated by divalent metal ion transporter 1 (DMT1) and ferroportin 1 (FPN1). Studies on human infants have shown that young infants cannot regulate iron absorption, whereas older infants can. Our studies on infant rat pups show that there is no regulation of DMT1 and FPN1 at young age, but that this develops at older age. These findings may explain adverse effects of iron supplementation on growth in young human infants. Zinc absorption in the small intestine is regulated by the transporters ZnT1, ZnT2, ZnT4 and Zip-4 and zinc status affects the expression of these transporters in an attempt to achieve zinc homeostasis. Copper absorption is regulated by the transporters Ctrl, Atp7A and Atp7B, and exposure to copper at early age affects the expression and cellular localization of these proteins, affecting copper uptake and transport. To date, most studies on homeostatic regulation of trace mineral absorption have been done in cell systems and animal models; further studies on human infants are needed. The consequences of trace element interactions during infancy also need to be investigated in more detail.

摘要

新生儿接触到的微量元素摄入量差异很大,但对于他们在体内平衡方面调节以适应这些摄入量的能力却知之甚少。近期在小肠中发现的几种金属离子转运蛋白,可能会增进我们对调节微量元素吸收的分子机制的理解。铁的吸收由二价金属离子转运蛋白1(DMT1)和铁转运蛋白1(FPN1)调节。对人类婴儿的研究表明,年幼婴儿无法调节铁的吸收,而年龄较大的婴儿则可以。我们对幼鼠的研究表明,年幼时DMT1和FPN1不受调节,但在年龄较大时会出现调节。这些发现可能解释了铁补充剂对年幼人类婴儿生长的不良影响。小肠中的锌吸收由转运蛋白ZnT1、ZnT2、ZnT4和Zip-4调节,锌状态会影响这些转运蛋白的表达,以维持锌的体内平衡。铜的吸收由转运蛋白Ctrl、Atp7A和Atp7B调节,早期接触铜会影响这些蛋白质的表达和细胞定位,从而影响铜的摄取和运输。迄今为止,大多数关于微量矿物质吸收体内平衡调节的研究都是在细胞系统和动物模型中进行的;还需要对人类婴儿进行进一步研究。婴儿期微量元素相互作用的后果也需要更详细地研究。

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