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首页> 美国卫生研究院文献>Nutrients >Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin as a Nutritive Source of Copper: Overview of the Current Data
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Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin as a Nutritive Source of Copper: Overview of the Current Data

机译：新生儿的铜代谢适应牛奶铜蓝蛋白作为铜的营养来源：当前数据概述

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摘要

Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a cofactor for cuproenzymes and its participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body, including copper absorption, distribution, and excretion. In ontogenesis, there are two types of copper metabolism, embryonic and adult, which maintain the balance of copper in each of these periods of life, respectively. In the liver cells, these types of metabolism are characterized by the specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter, and the proteins mediating ceruloplasmin metalation. In newborns, the molecular genetic mechanisms responsible for copper homeostasis and the ontogenetic switch from embryonic to adult copper metabolism are highly adapted to milk ceruloplasmin as a dietary source of copper. In the mammary gland cells, the level of ceruloplasmin gene expression and the alternative splicing of its pre-mRNA govern the amount of ceruloplasmin in the milk, and thus, the amount of copper absorbed by a newborn is controlled. In newborns, the absorption, distribution, and accumulation of copper are adapted to milk ceruloplasmin. If newborns are not breast-fed in the early stages of postnatal development, they do not have this natural control ensuring alimentary copper balance in the body. Although there is still much to be learned about the neonatal consequences of having an imbalance of copper in the motherewborn system, the time to pay attention to this problem has arrived because the neonatal misbalance of copper may provoke the development of copper-related disorders.
机译：铜可能是一种剧毒物质，由于其作为铜酶的辅助因子并参与信号传导途径，因此是一种重要的营养素。在哺乳动物中，肝脏是控制整个身体中铜代谢的中央器官，包括铜的吸收，分布和排泄。在本体发育中，铜代谢有两种类型，胚胎的和成年的，分别在生命的每个阶段维持铜的平衡。在肝细胞中，这些类型的新陈代谢的特征是编码铜蓝蛋白的基因（主要的细胞外铁氧化酶和铜转运蛋白）和介导铜蓝蛋白金属化的蛋白质的特定表达模式和活性水平。在新生儿中，负责铜体内稳态和从胚胎到成年铜代谢的个体发育转换的分子遗传机制高度适应于牛奶铜蓝蛋白作为饮食中铜的来源。在乳腺细胞中，铜蓝蛋白基因表达水平及其前mRNA的可变剪接决定了牛奶中铜蓝蛋白的含量，因此，新生儿的铜吸收量受到控制。在新生儿中，铜的吸收，分布和积累与牛奶中的铜蓝蛋白相适应。如果新生儿在产后发育的早期不进行母乳喂养，则他们没有这种自然控制能力，无法确保体内的营养铜平衡。尽管仍然有很多关于母体/新生儿系统中铜不平衡对新生儿的影响的研究，但由于新生儿铜的失衡可能会引起与铜有关的疾病的发展，因此现在是关注这一问题的时候了。

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