Department of Obstetrics and Gynaecology, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, Shaanxi, China.
Department of Obstetrics and Gynaecology, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, Shaanxi, China; Department of Obstetrics and Gynaecology, General Hospital of Tibet Military Region, Lhasa, 850007, Tibet, China.
Placenta. 2021 Oct;114:29-38. doi: 10.1016/j.placenta.2021.08.050. Epub 2021 Aug 16.
Children conceived by assisted reproductive technologies have a high risk of suffering from obstetrical complications and long-term health problems, but the related mechanisms are not fully understood. Normal placental function is closely linked with foetal growth and future health. Given the significance of glycogen metabolism in placentas, we investigated the effect of in vitro fertilization (IVF) on glycogen storage in placentas using a mouse model.
Mouse placentas were collected at E18.5 after natural mating or IVF, and the placental and foetal weights were recorded. The quantitative assay kit and histological staining were used to measure the glycogen content. Additionally, we detected the expression of multiple genes associated with glycogen synthesis/decomposition, glucose transporters, and the phosphorylation of Akt and Gsk3β.
Our findings showed that IVF resulted in a significantly increased mouse placental weight and enlarged junctional area. We found, compared to the control, excessive glycogen was accumulated in IVF placentas. However, we observed that multiple genes involved in glycogen generation (Gsk3b, Phka1, Phkb, Phkg1, and Phkg2) and glycogenolysis (Agl and Pygm) had lower mRNA levels in IVF placentas. Moreover, the expression levels of glycogen synthase, phosphorylase, Glut1, and Glut3 were significantly decreased in IVF placentas. The phosphorylation activities of Akt Ser473 and Gsk3β Ser9 were inhibited in IVF placentas.
IVF leads to enlarged mouse placentas with excessive glycogen storage in late pregnancy, and these abnormal changes may be associated with the activation of the Akt-Gsk3β pathway.
通过辅助生殖技术受孕的儿童患产科并发症和长期健康问题的风险较高，但相关机制尚未完全阐明。正常胎盘功能与胎儿生长和未来健康密切相关。鉴于糖元代谢在胎盘中的重要性，我们使用小鼠模型研究了体外受精（IVF）对胎盘糖元储存的影响。
自然交配或 IVF 后，在 E18.5 时收集小鼠胎盘，并记录胎盘和胎儿的重量。定量测定试剂盒和组织学染色用于测量糖元含量。此外，我们检测了与糖元合成/分解、葡萄糖转运体以及 Akt 和 Gsk3β磷酸化相关的多个基因的表达。
我们的研究结果表明，IVF 导致小鼠胎盘重量显著增加，连接区增大。与对照组相比，我们发现 IVF 胎盘中积累了过多的糖元。然而，我们观察到，参与糖元生成的多个基因（Gsk3b、Phka1、Phkb、Phkg1 和 Phkg2）和糖元分解（Agl 和 Pygm）在 IVF 胎盘中的 mRNA 水平较低。此外，IVF 胎盘中的糖原合酶、磷酸化酶、Glut1 和 Glut3 的表达水平显著降低。Akt Ser473 和 Gsk3β Ser9 的磷酸化活性在 IVF 胎盘中受到抑制。
IVF 导致妊娠晚期小鼠胎盘增大，糖元储存过多，这些异常变化可能与 Akt-Gsk3β 通路的激活有关。
