Fetoplacental vascular endothelial dysfunction as an early phenomenon in the programming of human adult diseases in subjects born from gestational diabetes mellitus or obesity in pregnancy.
Fetoplacental vascular endothelial dysfunction as an early phenomenon in the programming of human adult diseases in subjects born from gestational diabetes mellitus or obesity in pregnancy.
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DOI：
10.1155/2011/349286
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发表时间：
2011
影响因子：
--
通讯作者：
Sobrevia L
中科院分区：
文献类型：
--
作者：
Leiva A;Pardo F;Ramírez MA;Farías M;Casanello P;Sobrevia L
妊娠期糖尿病（GDM）和妊娠期肥胖（OP）是与胎盘血管功能障碍相关的病理状况，伴随胎儿胎盘微血管和大血管内皮的代谢变化。这些改变被视为阳离子氨基酸转运蛋白和内皮一氧化氮合酶异构体的异常表达和活性，即“内皮L-精氨酸/一氧化氮信号通路”。多项研究表明，内源性核苷腺苷与胰岛素以及可能的精氨酸酶一起是 GDM 的相关因素，但有关它们在 OP 相关胎盘血管改变中的作用的信息却少之又少。有令人信服的证据表明，GDM 和 OP 容易使胎盘内皮进入“代谢状态改变”，从而导致出生时出现的胎儿编程，这种现象与未来慢性疾病的发展相关。本文提出，这种病理状态可以被认为是一种代谢标志物，可以预测成年后疾病的发生，如心血管疾病、肥胖、糖尿病（包括妊娠糖尿病）和代谢综合征。
Gestational diabetes mellitus (GDM) and obesity in pregnancy (OP) are pathological conditions associated with placenta vascular dysfunction coursing with metabolic changes at the fetoplacental microvascular and macrovascular endothelium. These alterations are seen as abnormal expression and activity of the cationic amino acid transporters and endothelial nitric oxide synthase isoform, that is, the “endothelial L-arginine/nitric oxide signalling pathway.” Several studies suggest that the endogenous nucleoside adenosine along with insulin, and potentially arginases, are factors involved in GDM-, but much less information regards their role in OP-associated placental vascular alterations. There is convincing evidence that GDM and OP prone placental endothelium to an “altered metabolic state” leading to fetal programming evidenced at birth, a phenomenon associated with future development of chronic diseases. In this paper it is suggested that this pathological state could be considered as a metabolic marker that could predict occurrence of diseases in adulthood, such as cardiovascular disease, obesity, diabetes mellitus (including gestational diabetes), and metabolic syndrome.
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影响因子：
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作者：
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