Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China; Institute of Neuroscience, Translational Medicine Institute, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Department of Endocrinology and Second Department of Geriatrics, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Nutr Metab Cardiovasc Dis. 2022 Mar;32(3):692-702. doi: 10.1016/j.numecd.2021.12.018. Epub 2021 Dec 25.
Placental lipid transport is altered in women with high prepregnancy body mass index (pre-BMI) or gestational diabetes (GDM), which consequently affects foetal growth. However, the interaction of maternal overweight (OW) and GDM on placental lipid metabolism and possible adaptations are less studied. We aimed to examine whether maternal OW or GDM is the main factor disrupting placental lipid processing in human term placenta.
A total of 152 lean (18.5 ≤ pre-BMI ≤ 23.9 kg/m) and OW (24 ≤ pre-BMI ≤ 27.9 kg/m) pregnant women with or without GDM with a scheduled delivery by caesarean section were recruited. Maternal venous blood samples were used to measure metabolic parameters during pregnancy. Term placentas and cord blood were collected at delivery to determine placental lipid metabolism and foetal circulating lipid levels. Maternal OW significantly increased the placental mRNA expression of genes involved in lipid metabolism (FAT/CD36, FATP1, FATP4, FATP6, and PPAR-α), elevated placental lipid content (triglyceride, cholesterol), enhanced placental mTORC1-rpS6 and ERK1/2 signalling, increased cord blood insulin levels and birth weight. Neonatal birth weight was positively correlated with maternal pre-BMI, placental ERK1/2 signalling and cord blood insulin. There was an interaction between OW and GDM in regulating key placental fuel transport and storage gene expression (LPL, FATP6, FABP7, PPAR-α, PPAR-β, PPAR-γ, IR-β, GLUT1, SNAT2, SNAT4, and LAT1).
Maternal OW mainly affects placental lipid metabolism, which may contribute to foetal overgrowth and may impact long-term offspring health. GDM plays a less significant role in affecting placental lipid transfer and other mechanisms may be involved.
孕前体重指数（pre-BMI）较高或患有妊娠期糖尿病（GDM）的女性其胎盘脂质转运发生改变，进而影响胎儿生长。然而，母体超重（OW）和 GDM 对胎盘脂质代谢及可能的适应性的相互作用研究较少。本研究旨在探讨母体 OW 或 GDM 是否为破坏人足月胎盘中胎盘脂质处理的主要因素。
共纳入 152 例计划行剖宫产分娩的孕妇，其中瘦孕妇（18.5≤pre-BMI≤23.9kg/m²）和 OW 孕妇（24≤pre-BMI≤27.9kg/m²）各 76 例，且这些孕妇均不患有 GDM 或患有 GDM。孕期采集母体静脉血样以检测代谢参数。分娩时采集胎盘和脐血以测定胎盘脂质代谢和胎儿循环脂质水平。母体 OW 显著增加了与脂质代谢相关的基因（FAT/CD36、FATP1、FATP4、FATP6 和 PPAR-α）在胎盘组织中的 mRNA 表达，增加了胎盘脂质含量（甘油三酯、胆固醇），增强了胎盘 mTORC1-rpS6 和 ERK1/2 信号，升高了脐血胰岛素水平和新生儿出生体重。新生儿出生体重与母体 pre-BMI、胎盘 ERK1/2 信号和脐血胰岛素呈正相关。OW 和 GDM 对关键胎盘燃料转运和储存基因表达（LPL、FATP6、FABP7、PPAR-α、PPAR-β、PPAR-γ、IR-β、GLUT1、SNAT2、SNAT4 和 LAT1）的调控存在交互作用。
母体 OW 主要影响胎盘脂质代谢，这可能导致胎儿过度生长，并可能影响后代的长期健康。GDM 对胎盘脂质转运的影响作用较小，可能涉及其他机制。
