Maternal nutrition and fetal development

Maternal nutrition and fetal development
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DOI:
10.1093/jn/134.9.2169
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发表时间:
2004-09-01
影响因子:
4.2
通讯作者:
Spencer, TE
Spencer, TE
中科院分区:
医学2区
文献类型:
--
作者:
Wu, GY;Bazer, FW;Spencer, TE

文献摘要

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营养是改变胎儿基因组表达的主要宫内环境因素,并可能产生终身影响。这种现象被称为“胎儿编程”,导致了最近的“成人疾病的胎儿起源”理论。也就是说,胎儿营养和内分泌状态的改变可能导致发育适应性改变,永久改变后代的结构,生理和代谢,从而使个体在成年后易患代谢,内分泌和心血管疾病。动物研究表明,母亲营养不足和营养过剩都会减少胎盘-胎儿血流,阻碍胎儿生长。胎盘合成一氧化氮(一种主要的血管扩张剂和血管生成因子)和多胺(DNA和蛋白质合成的关键调节剂)的受损可能为宫内生长迟缓提供统一的解释,以应对具有相同妊娠结局的两种极端营养问题。越来越多的证据表明,母亲的营养状况可以改变胎儿基因组的表观遗传状态(通过DNA甲基化和组蛋白修饰稳定改变基因表达)。这可能为母体营养对胎儿编程和基因组印记的影响提供了分子机制。促进最佳营养不仅可以确保最佳的胎儿发育,还可以降低成年人患慢性疾病的风险。
Nutrition is the major intrauterine environmental factor that alters expression of the fetal genome and may have lifelong consequences. This phenomenon, termed "fetal programming," has led to the recent theory of "fetal origins of adult disease." Namely, alterations in fetal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology, and metabolism of the offspring, thereby predisposing individuals to metabolic, endocrine, and cardiovascular diseases in adult life. Animal studies show that both maternal undernutrition and overnutrition reduce placental-fetal blood flows and stunt fetal growth. Impaired placental syntheses of nitric oxide (a major vasodilator and angiogenesis factor) and polyamines (key regulators of DNA and protein synthesis) may provide a unified explanation for intrauterine growth retardation in response to the 2 extremes of nutritional problems with the same pregnancy outcome. There is growing evidence that maternal nutritional status can alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome. This may provide a molecular mechanism for the impact of maternal nutrition on both fetal programming and genomic imprinting. Promoting optimal nutrition will not only ensure optimal fetal development, but will also reduce the risk of chronic diseases in adults.