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内皮型一氧化氮合酶缺乏导致胎盘代谢异常。

Endothelial nitric oxide deficiency results in abnormal placental metabolism.

机构信息

Department of Chemistry, Memorial University of Newfoundland, St. John's, Newfoundland, Canada.

Department of Chemistry, Memorial University of Newfoundland, St. John's, Newfoundland, Canada; Discipline of Radiology, Memorial University of Newfoundland, St. John's, Newfoundland, Canada.

出版信息

Placenta. 2022 Oct;128:36-38. doi: 10.1016/j.placenta.2022.08.013. Epub 2022 Aug 29.

DOI:10.1016/j.placenta.2022.08.013
PMID:36058049
Abstract

Placental metabolism determines the amount of nutrients available to the fetus and may be altered in pregnancies complicated by fetal growth restriction (FGR). To study which metabolites are associated with FGR, we performed H high-resolution magic angle spinning magnetic resonance spectroscopy of placental tissue from endothelial nitric oxide synthase knockout (eNOS KO) mice, a model of FGR, and C57BL/6J controls at embryonic day 17.5 (n = 24/genotype). The relative concentration of glucose was increased in the placentas of eNOS KO mice compared to controls (p = 0.006). This study highlights the potential for glucose as a biomarker of abnormal placental metabolism that leads to FGR.

摘要

胎盘代谢决定了胎儿可获得的营养物质的数量,并且在胎儿生长受限(FGR)的妊娠中可能会发生改变。为了研究哪些代谢物与 FGR 相关,我们在胚胎期 17.5 天时对内皮型一氧化氮合酶敲除(eNOS KO)小鼠(FGR 模型)和 C57BL/6J 对照的胎盘组织进行了 H 高分辨率魔角旋转磁共振波谱分析(n = 24/基因型)。与对照组相比,eNOS KO 小鼠的胎盘葡萄糖浓度相对增加(p = 0.006)。这项研究强调了葡萄糖作为异常胎盘代谢导致 FGR 的生物标志物的潜力。

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Parental sex-dependent effects of either maternal or paternal eNOS deficiency on the offspring's phenotype without transmission of the parental eNOS deficiency to the offspring.母源或父源内皮型一氧化氮合酶(eNOS)缺乏对后代表型的亲代性别依赖性影响,且亲代的eNOS缺乏不会传递给后代。
Front Physiol. 2023 Dec 19;14:1306178. doi: 10.3389/fphys.2023.1306178. eCollection 2023.
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