Fetal growth restriction and postnatal development

Fetal growth restriction and postnatal development
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DOI:
10.1196/annals.1365.047
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发表时间:
2006-01-01
期刊:
WOMEN'S HEALTH AND DISEASE: GYNECOLOGIC, ENDOCRINE, AND REPRODUCTIVE ISSUES
影响因子:
--
通讯作者:
Nicolaides, Kypros
Nicolaides, Kypros
中科院分区:
其他
文献类型:
--
作者:
Eleftheriades, Makarios;Creatsas, George;Nicolaides, Kypros

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遗传结构和宫内环境之间的相互作用决定了胎儿的生长和发育,并影响成年后对某些疾病的易感性。来自动物和人类研究的数据表明,产前和产后早期营养不良可以编程下丘脑-垂体-肾上腺轴(HPA轴),改变一生中对压力源的神经内分泌反应。子宫胎盘灌注受损导致胎儿生长受限(FGR)。在FGR中,有证据表明慢性低氧血症和代谢、内分泌和血液学参数的改变,与饥饿相符。此外,FGR与围产期死亡率增加有关,在幸存者中,成年后对糖尿病和心血管疾病的易感性增加。有证据表明,出生后早期的生长加速,通常被认为是可取的,可能会加剧晚年的代谢功能障碍。
The interaction between genetic constitution and in utero environment determines fetal growth and development and influences the susceptibility to certain disorders in adulthood. Data from both animal and human studies indicate that prenatal and early postnatal malnutrition can program the hypothalamus-pituitary-adrenal axis (HPA axis), altering neuroendocrine response to stressors throughout lifetime. Impaired uteroplacental perfusion results in fetal growth restriction (FGR). In FGR there is evidence of chronic hypoxemia and alterations in metabolic, endocrine, and hematological parameters, compatible with starvation. Furthermore, FGR is associated with increased perinatal mortality and in the survivors there is increased susceptibility to diabetes and cardiovascular disease in adulthood. There is evidence that early postnatal growth acceleration, which would normally be considered desirable, may exacerbate metabolic dysfunction in later life.