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Maternal metabolic conditions and risk for autism and other neurodevelopmental disorders.母体代谢状况与自闭症和其他神经发育障碍的风险。
Pediatrics. 2012 May;129(5):e1121-8. doi: 10.1542/peds.2011-2583. Epub 2012 Apr 9.
2
A trigger-based design for evaluating the safety of in utero antiretroviral exposure in uninfected children of human immunodeficiency virus-infected mothers.基于触发因素的设计用于评估人类免疫缺陷病毒感染母亲所生未感染儿童的宫内抗逆转录病毒暴露的安全性。
Am J Epidemiol. 2012 May 1;175(9):950-61. doi: 10.1093/aje/kwr401. Epub 2012 Apr 6.
3
DNA methylation in peripheral blood measured by LUMA is associated with breast cancer in a population-based study.基于人群的研究表明,外周血中的 DNA 甲基化(由 LUMA 测定)与乳腺癌有关。
FASEB J. 2012 Jun;26(6):2657-66. doi: 10.1096/fj.11-197251. Epub 2012 Feb 27.
4
Exposure to gestational diabetes mellitus and low socioeconomic status: effects on neurocognitive development and risk of attention-deficit/hyperactivity disorder in offspring.暴露于妊娠期糖尿病和低社会经济地位:对后代神经认知发育及注意力缺陷/多动障碍风险的影响。
Arch Pediatr Adolesc Med. 2012 Apr;166(4):337-43. doi: 10.1001/archpediatrics.2011.784. Epub 2012 Jan 2.
5
Childhood cognitive ability: relationship to gestational diabetes mellitus in India.儿童认知能力:与印度妊娠期糖尿病的关系。
Diabetologia. 2010 Oct;53(10):2134-8. doi: 10.1007/s00125-010-1847-0. Epub 2010 Jul 8.
6
Development and function of trophoblast giant cells in the rodent placenta.啮齿动物胎盘中滋养层巨细胞的发育与功能
Int J Dev Biol. 2010;54(2-3):341-54. doi: 10.1387/ijdb.082768dh.
7
Perinatal risk factors for childhood obesity and metabolic dysregulation.围产期儿童肥胖和代谢失调的风险因素。
Am J Clin Nutr. 2009 Nov;90(5):1303-13. doi: 10.3945/ajcn.2008.27416. Epub 2009 Sep 16.
8
DNA methylation differences after exposure to prenatal famine are common and timing- and sex-specific.暴露于产前饥荒后 DNA 甲基化差异普遍存在且具有时间和性别特异性。
Hum Mol Genet. 2009 Nov 1;18(21):4046-53. doi: 10.1093/hmg/ddp353. Epub 2009 Aug 4.
9
Fetuses of obese mothers develop insulin resistance in utero.肥胖母亲的胎儿在子宫内就会出现胰岛素抵抗。
Diabetes Care. 2009 Jun;32(6):1076-80. doi: 10.2337/dc08-2077.
10
Gestational diabetes hinders language development in offspring.妊娠期糖尿病会阻碍后代的语言发育。
Pediatrics. 2008 Nov;122(5):e1073-9. doi: 10.1542/peds.2007-3028.

母体妊娠期糖尿病、子痫前期和肥胖症与胎盘和脐带血的全球甲基化。

Global methylation in the placenta and umbilical cord blood from pregnancies with maternal gestational diabetes, preeclampsia, and obesity.

机构信息

1Department of Psychology, Queens College, CUNY, Flushing, NY, USA.

出版信息

Reprod Sci. 2014 Jan;21(1):131-7. doi: 10.1177/1933719113492206. Epub 2013 Jun 13.

DOI:10.1177/1933719113492206
PMID:23765376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3857768/
Abstract

Emerging evidence indicates that maternal medical risk during pregnancy, such as gestational diabetes mellitus (GDM), preeclampsia, and obesity, predisposes the offspring to suboptimal development. However, the underlying biological/epigenetic mechanism in utero is still unknown. The current pilot study (N = 50) compared the levels of global methylation in the placenta and umbilical cord blood among women with and without each risk condition (GDM, preeclampsia, and obesity) and explored whether the levels of global methylation were associated with fetal/infant growth. Results show that global methylation levels in the placenta were lower in patients with gestational diabetes (P = .003) and preeclampsia (P = .05) but higher with obesity (P = .01). Suggestive negative associations were found between global methylation level in the placenta and infant body length and head circumference. While preliminary, it is possible that the placenta tissue, but not umbilical cord blood, may be epigenetically programmed by maternal GDM, preeclampsia, and obesity to carry out its own specific functions that influence fetal growth.

摘要

新出现的证据表明,孕妇在妊娠期间的医疗风险,如妊娠糖尿病(GDM)、先兆子痫和肥胖,使后代发育不良的风险增加。然而,子宫内潜在的生物学/表观遗传机制尚不清楚。本研究(N=50)比较了患有和不患有每种风险条件(GDM、先兆子痫和肥胖)的女性胎盘和脐血中的全球甲基化水平,并探讨了全球甲基化水平是否与胎儿/婴儿生长有关。结果表明,患有妊娠糖尿病(P=0.003)和先兆子痫(P=0.05)的患者胎盘的全球甲基化水平较低,但肥胖患者(P=0.01)的水平较高。胎盘组织中的全球甲基化水平与婴儿的身长和头围呈负相关。虽然这只是初步研究,但胎盘组织而不是脐血可能会受到母体 GDM、先兆子痫和肥胖的表观遗传编程,以执行其自身特定的功能,从而影响胎儿的生长。