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首页> 外文期刊>Placenta >Placental amino acid transport and placental leptin resistance in pregnancies complicated by maternal obesity.
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Placental amino acid transport and placental leptin resistance in pregnancies complicated by maternal obesity.

机译:妊娠期妊娠期妊娠期胎盘氨基酸输送和胎盘瘦素抵抗。

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摘要

HYPOTHESIS AND STUDY OBJECTIVES: We hypothesized that maternal obesity is associated with increased placental amino acid transport and hyperleptinemia. Our objectives were to study placental amino acid transport and the effect of leptin on placental amino acid transport in vitro in the setting of maternal obesity. MATERIALS AND METHODS: Seven lean, BMI at entry 22.4, and seven obese, BMI at entry 31.5 (p < 0.001), pregnant women were studied at 39 weeks. We measured baseline and leptin-stimulated placental system A sodium-dependent neutral amino acid transporter (SNAT) activity, placental immunoreactive protein expression of SNAT, leptin and leptin receptor, and maternal and fetal plasma leptin concentrations, with significance set at p
机译:假设和研究目标:我们假设母体肥胖与增加的胎盘氨基酸输送和高层血症有关。我们的目标是研究胎盘氨基酸输送和瘦素对孕产妇肥胖的体外胎盘氨基酸输送的影响。材料和方法:七个瘦,BMI入口22.4,七个肥胖,BMI在入口31.5(P <0.001),孕妇在39周内进行了研究。我们测量了基线和瘦素刺激的胎盘系统钠依赖性中性氨基酸转运蛋白(SNAT)活性,SnAT,瘦素和瘦素受体的胎盘免疫反应性蛋白表达,以及母体和胎儿血浆瘦蛋白浓度,具有P <或=的显着性0.05。主要结果措施是胎盘SNAT活动。结果:肥胖基团的胎盘SNAT活性(P = 0.005),母体高葡萄肿血症(P = 0.01)和瘦蛋白受体的单胞生殖性表达减少(P = 0.01)和SNAT-4(P <0.001)。与肥胖基团相比,瘦蛋白在瘦蛋白中显着刺激胎盘氨基酸摄取。母体体重增加和后代出生体重在组之间没有差异。结论:母亲肥胖症伴随着与孕产妇高白葡萄肿瘤和胎盘瘦蛋白抗性相关的胎盘SNAT活性,尽管存在适当的母体体重增加和通常种植的新生儿。这些发现表明改变的胎盘功能可能对肥胖孕妇的临床意义。

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