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肾单位数量的宫内编程:重新审视胎儿期缺陷

Intrauterine programming of nephron number: the fetal flaw revisited.

作者信息

Marchand M C, Langley-Evans S C

机构信息

Human Nutrition and Metabolism Group, University College Northampton, United Kingdom.

出版信息

J Nephrol. 2001 Sep-Oct;14(5):327-31.

PMID:11730264
Abstract

A broad range of epidemiological evidence supports the hypothesis that risk of essential hypertension, coronary heart disease and non-insulin dependent diabetes is, in part, determined before birth. This phenomenon, termed programming, is now the subject of intensive investigation in order to determine possible underlying mechanisms. It is widely accepted that maternal nutritional status in pregnancy is a major programming influence upon the fetus. This review considers the hypothesis that nephron number in humans is determined by prenatal nutrition. An increasing number of human studies indicate that the developing kidney is particularly vulnerable to the adverse effects of fetal growth retarding influences. In animals, growth retarding diets or other insults which have an impact upon the development of cardiovascular functions, also appear to impact upon nephron number. However, it is possible that hypertension and reduced renal reserve merely coincide and are not causally associated.

摘要

大量的流行病学证据支持这样一种假说,即原发性高血压、冠心病和非胰岛素依赖型糖尿病的风险部分在出生前就已确定。这种现象被称为程序化,目前正受到深入研究,以确定可能的潜在机制。人们普遍认为,孕期母亲的营养状况是对胎儿的主要程序化影响因素。本综述探讨了人类肾单位数量由产前营养决定这一假说。越来越多的人体研究表明,发育中的肾脏特别容易受到胎儿生长迟缓影响的不利作用。在动物中,限制生长的饮食或其他对心血管功能发育有影响的损伤,似乎也会影响肾单位数量。然而,高血压和肾储备减少可能只是同时出现,并无因果关系。

相似文献

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Intrauterine programming of nephron number: the fetal flaw revisited.肾单位数量的宫内编程:重新审视胎儿期缺陷
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2
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Role of the placenta in fetal programming: underlying mechanisms and potential interventional approaches.胎盘在胎儿编程中的作用:潜在机制与可能的干预方法。
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Normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat.正常的泌乳环境可恢复大鼠胎盘受限后的肾单位数量并预防高血压。
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