Obstetrics and Prenatal Medicine, Gynecology and Obstetrics, University Hospital Frankfurt, J. W. Goethe-University, Theodor Stern-Kai 7, 60590, Frankfurt, Germany.
Arch Gynecol Obstet. 2024 Jun;309(6):2279-2288. doi: 10.1007/s00404-024-07462-w. Epub 2024 Mar 18.
The prevalence of maternal obesity rapidly increases, which represents a major public health concern worldwide. Maternal obesity is characteristic by metabolic dysfunction and chronic inflammation. It is associated with health problems in both mother and offspring. Increasing evidence indicates that the placenta is an axis connecting maternal obesity with poor outcomes in the offspring. In this brief review, we have summarized the current data regarding deregulated placental function in maternal obesity. The data show that maternal obesity induces numerous placental defects, including lipid and glucose metabolism, stress response, inflammation, immune regulation and epigenetics. These placental defects affect each other and result in a stressful intrauterine environment, which transduces and mediates the adverse effects of maternal obesity to the fetus. Further investigations are required to explore the exact molecular alterations in the placenta in maternal obesity, which may pave the way to develop specific interventions for preventing epigenetic and metabolic programming in the fetus.
孕妇肥胖的患病率迅速增加,这是全球主要的公共卫生关注点。孕妇肥胖的特点是代谢功能障碍和慢性炎症。它与母婴健康问题都有关联。越来越多的证据表明,胎盘是连接孕妇肥胖与后代不良结局的轴心。在这篇简要综述中,我们总结了目前关于孕妇肥胖时胎盘功能失调的相关数据。这些数据表明,孕妇肥胖会导致许多胎盘缺陷,包括脂质和葡萄糖代谢、应激反应、炎症、免疫调节和表观遗传学。这些胎盘缺陷相互影响,导致宫内环境紧张,从而将孕妇肥胖的不良影响传递和介导给胎儿。需要进一步的研究来探索孕妇肥胖时胎盘的确切分子变化,这可能为开发预防胎儿表观遗传和代谢编程的特定干预措施铺平道路。