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糖尿病相关先天性畸形的发病机制。

The pathogenesis of diabetes-associated congenital malformations.

作者信息

Reece E A, Eriksson U J

机构信息

Department of Obstetrics, Gynecology and Reproductive Sciences, Temple University School of Medicine, Philadelphia, Pennsylvania USA.

出版信息

Obstet Gynecol Clin North Am. 1996 Mar;23(1):29-45. doi: 10.1016/s0889-8545(05)70243-6.

DOI:10.1016/s0889-8545(05)70243-6
PMID:8684783
Abstract

Congenital malformations convey a major financial and social burden to society. Epidemiologic, clinical, and animal studies indicate that these malformations occur in early pregnancy, are influenced by an aberrant metabolic fuel milieu, and seem to result from a combination of more than one factor acting synchronously. Unfortunately, during the critical period of organogenesis, the pregnancy is hardly recognizable, making evaluation and study of relevant maternal embryonic parameters extremely difficult. Additionally, there are obvious limitations to human study for technical and ethical reasons. Animal experimentation, however, has demonstrated that these malformations can be produced in many vertebrates and are similar to those seen in humans. The mechanism for induction of dysmorphogenesis in experimental diabetic pregnancy has been shown to include generation of free oxygen radicals and are associated with alterations in the embryonic levels of arachidonic acid, prostaglandins, and myo-inositol. Most of the earlier experimental studies focused on defects at the level of the embryo excluding the extraembryonic membranes. Current investigations provide evidence that the yolk sac has an integral role in diabetic embryopathy. The experimental use of several different compounds, such as arachidonic acid, myo-inositol, and antioxidants, offers significant promise for the future in possibly serving as a pharmacologic prophylaxis against diabetic embryopathy.

摘要

先天性畸形给社会带来了巨大的经济和社会负担。流行病学、临床及动物研究表明,这些畸形发生在妊娠早期,受异常代谢燃料环境影响,似乎是多种因素同步作用的结果。不幸的是,在器官发生的关键时期,妊娠很难被察觉,这使得评估和研究相关母体胚胎参数极为困难。此外,出于技术和伦理原因,人体研究存在明显局限性。然而,动物实验表明,这些畸形可在许多脊椎动物中产生,且与人类所见畸形相似。实验性糖尿病妊娠中诱导畸形发生的机制已表明包括自由基的产生,并与胚胎中花生四烯酸、前列腺素和肌醇水平的改变有关。大多数早期实验研究集中在胚胎水平的缺陷,不包括胚外膜。目前的研究提供了证据表明卵黄囊在糖尿病胚胎病中起重要作用。几种不同化合物,如花生四烯酸、肌醇和抗氧化剂的实验应用,为未来作为预防糖尿病胚胎病的药物预防提供了重大希望。

相似文献

1
The pathogenesis of diabetes-associated congenital malformations.糖尿病相关先天性畸形的发病机制。
Obstet Gynecol Clin North Am. 1996 Mar;23(1):29-45. doi: 10.1016/s0889-8545(05)70243-6.
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The role of free radicals and membrane lipids in diabetes-induced congenital malformations.自由基和膜脂在糖尿病诱导的先天性畸形中的作用。
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New development of the yolk sac theory in diabetic embryopathy: molecular mechanism and link to structural birth defects.糖尿病胚胎病中卵黄囊理论的新进展:分子机制及其与结构性出生缺陷的关联
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2
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New development of the yolk sac theory in diabetic embryopathy: molecular mechanism and link to structural birth defects.
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Use of a murine embryonic stem cell line that is sensitive to high glucose environment to model neural tube development in diabetic pregnancy.利用对高糖环境敏感的小鼠胚胎干细胞系来模拟糖尿病妊娠中的神经管发育。
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