首页> 美国卫生研究院文献>Frontiers in Pediatrics >ExtraUterine Growth Restriction (EUGR) in Preterm Infants: Growth Patterns Nutrition and Epigenetic Markers. A Pilot Study
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ExtraUterine Growth Restriction (EUGR) in Preterm Infants: Growth Patterns Nutrition and Epigenetic Markers. A Pilot Study

机译:早产儿子宫外生长限制(EUGR):生长方式营养和表观遗传标记。初步研究

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摘要

>Background/Aims: IntraUterine (IUGR) and ExtraUterine Growth Restriction (EUGR) may induce reprogramming mechanisms, finalized to survive before and after birth. Nutritional factors and other environmental signals could regulate gene expression through epigenetic modification, but the molecular mechanisms involved are not yet well understood. Epigenetic mechanisms could be considered as a bridge between environmental stimuli and long lasting phenotype, acquired during the intrauterine life and the first weeks of life. Our aim was to investigate the relationship between growth patterns, nutritional determinants, and epigenetic pathways.>Methods: We enrolled 38 newborns admitted to Neonatal Intensive Care Unit (NICU) at University Hospital of Pisa. Gestational age at birth was <34 weeks and post-menstrual age (PMA) was 36–42 weeks at discharge. We excluded infants with malformations or clinical syndromes. EUGR was defined as the reduction in weight z score between birth and discharge >1 SD. We also evaluated DNA methylation of Imprinting Centre 1 (IC1) at birth and at discharge.>Results: We observed a decrease in SD of weight and head circumference mainly during the first weeks of life. We found a correlation between EUGR for weight and for head circumference and an increased IC1 methylation (p = 0.018 and p = 0.0028, respectively). We observed a relationship between reduced protein and lipid intake and IC1 hypermethylation (p = 0.009 and p = 0.043, respectively).>Conclusion: IC1 hypermethylation could be a reprogramming mechanism to promote a catch-up growth, by means of an increased Insulin-like growth factor 2 (IGF2) expression, that may have potential effects on metabolic homeostasis later in life.
机译:>背景/目标:子宫内(IUGR)和子宫外生长限制(EUGR)可能会诱导重编程机制,并最终确定其在出生前和出生后均可存活。营养因素和其他环境信号可以通过表观遗传修饰来调控基因表达,但是所涉及的分子机制尚未得到很好的理解。表观遗传机制可以被认为是在子宫内生命和生命的最初几周中获得的环境刺激和持久表型之间的桥梁。我们的目的是研究生长方式,营养决定因素和表观遗传途径之间的关系。>方法:我们招募了38名在比萨大学医院新生儿重症监护室(NICU)住院的新生儿。出生时的胎龄小于34周,出院时的月经年龄(PMA)为36-42周。我们排除了畸形或临床综合征的婴儿。 EUGR被定义为出生与出院之间体重z得分的减少> 1 SD。我们还评估了印迹中心1(IC1)在出生和出院时的DNA甲基化。>结果:我们观察到体重和头围的SD下降主要在生命的最初几周内。我们发现EUGR的重量和头围与IC1甲基化增加(分别为p = 0.018和p = 0.0028)之间具有相关性。我们观察到蛋白质和脂质摄入减少与IC1高度甲基化之间的关系(分别为p = 0.009和p = 0.043)。>结论: IC1高度甲基化可能是通过促进追赶性生长的重编程机制。胰岛素样生长因子2(IGF2)表达增加的一种方式,可能对生命后期的代谢稳态产生潜在影响。

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