Update: Consequences of Abnormal Fetal Growth

Update: Consequences of Abnormal Fetal Growth
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DOI:
10.1210/jc.2011-2741
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发表时间:
2012-03-01
影响因子:
5.8
通讯作者:
Chernausek, Steven D.
Chernausek, Steven D.
中科院分区:
医学2区
文献类型:
--
作者:
Chernausek, Steven D.

文献摘要

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宫内生长受限(IUGR)在世界范围内普遍存在,并以多种方式影响儿童和成人。这些包括2型糖尿病的易感性、代谢综合征、心血管疾病、身材持续下降以​​及青春期模式的可能变化。对最近文献的回顾证实,出生时小于胎龄的代谢影响在很小的时候就很明显,并且随着年龄的增长而持续存在,并且因肥胖而加剧。此外,生命最初几年的生长模式对一个人以后的健康有重大影响,体重增加的人未来代谢功能障碍的风险最大。外源性人类生长激素治疗用于提高出生时小于胎龄后仍身材矮小的儿童的身高,但个体的反应仍然存在差异且难以预测。 IUGR 儿童代谢编程的机制才刚刚开始被探索。 IUGR 似乎会导致 DNA 甲基化的广泛变化,并且可能在各种胎儿组织中发现 IUGR 的特定“表观遗传特征”。面临的挑战是将这种改变与基因表达的改变以及最终成年期的代谢异常联系起来,它代表了该领域研究的前沿之一。 (临床内分泌代谢杂志 97:689-695, 2012)
Intrauterine growth restriction (IUGR) is prevalent worldwide and affects children and adults in multiple ways. These include predisposition to type 2 diabetes mellitus, the metabolic syndrome, cardiovascular disease, persistent reduction in stature, and possibly changes in the pattern of puberty. A review of recent literature confirms that the metabolic effects of being born small for gestational age are evident in the very young, persist with age, and are amplified by adiposity. Furthermore, the pattern of growth in the first few years of life has a significant bearing on a person's later health, with those that show increasing weight gain being at the greatest risk for future metabolic dysfunction. Treatment with exogenous human GH is used to improve height in children who remain short after being small for gestational age at birth, but the response of individuals remains variable and difficult to predict. The mechanisms involved in the metabolic programming of IUGR children are just beginning to be explored. It appears that IUGR leads to widespread changes in DNA methylation and that specific "epigenetic signatures" for IUGR are likely to be found in various fetal tissues. The challenge is to link such alterations with modifications in gene expression and ultimately the metabolic abnormalities of adulthood, and it represents one of the frontiers for research in the field. (J Clin Endocrinol Metab 97:689-695, 2012)