Placental Endocrine Activity: Adaptation and Disruption of Maternal Glucose Metabolism in Pregnancy and the Influence of Fetal Sex.

Placental Endocrine Activity: Adaptation and Disruption of Maternal Glucose Metabolism in Pregnancy and the Influence of Fetal Sex.
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DOI:
10.3390/ijms222312722
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发表时间:
2021-11-24
影响因子:
5.6
通讯作者:
Hiden U
Hiden U
中科院分区:
生物学2区
文献类型:
--
作者:
Stern C;Schwarz S;Moser G;Cvitic S;Jantscher-Krenn E;Gauster M;Hiden U

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胎盘是一个内分泌胎儿器官,它分泌过多的类固醇和蛋白激素,代谢蛋白,生长因子和细胞因子,以适应母体生理怀孕。胎儿生长的核心是营养的供应,首先是葡萄糖。因此,在怀孕期间,母体胰岛素抵抗出现,这提高了母体血糖水平,从而确保发育中的胎儿有足够的葡萄糖供应。同时,母体β细胞质量和功能增加,以补偿较高的胰岛素需求。这些适应也受到胎盘内分泌功能的调节。过度的胰岛素抵抗或不能增加胰岛素产生,从而破坏妊娠介导的葡萄糖代谢的生理调节,并可能导致母体妊娠糖尿病(GDM)。越来越多的证据表明,这种对母体葡萄糖代谢的适应在怀女孩的怀孕与怀男孩的怀孕之间是不同的。此外,发生GDM的风险因胎儿性别而异。胎盘源激素和生物活性蛋白的性别差异,适应和调节母体葡萄糖代谢,可能有助于这种性别二型性。本文综述了胎盘源性因子对母体葡萄糖代谢的适应和适应不良,并强调了这一调节网络的性别差异。
The placenta is an endocrine fetal organ, which secretes a plethora of steroid- and proteo-hormones, metabolic proteins, growth factors, and cytokines in order to adapt maternal physiology to pregnancy. Central to the growth of the fetus is the supply with nutrients, foremost with glucose. Therefore, during pregnancy, maternal insulin resistance arises, which elevates maternal blood glucose levels, and consequently ensures an adequate glucose supply for the developing fetus. At the same time, maternal β-cell mass and function increase to compensate for the higher insulin demand. These adaptations are also regulated by the endocrine function of the placenta. Excessive insulin resistance or the inability to increase insulin production accordingly disrupts physiological modulation of pregnancy mediated glucose metabolism and may cause maternal gestational diabetes (GDM). A growing body of evidence suggests that this adaptation of maternal glucose metabolism differs between pregnancies carrying a girl vs. pregnancies carrying a boy. Moreover, the risk of developing GDM differs depending on the sex of the fetus. Sex differences in placenta derived hormones and bioactive proteins, which adapt and modulate maternal glucose metabolism, are likely to contribute to this sexual dimorphism. This review provides an overview on the adaptation and maladaptation of maternal glucose metabolism by placenta-derived factors, and highlights sex differences in this regulatory network.
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