Department of Obstetrics, Division of Obstetrics and Gynecology, Rikshospitalet, Oslo University Hospital, 0424, Oslo, Norway.
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0318, Oslo, Norway.
J Endocrinol Invest. 2022 Nov;45(11):2105-2121. doi: 10.1007/s40618-022-01842-2. Epub 2022 Jul 4.
Placental weight (PW) has been found to mediate the main effect of maternal BMI on fetal size. Still, the BMI-PW association is poorly understood. Therefore, we aimed to explore potential explanatory variables, including gestational weight gain (GWG), early- and late-pregnancy circulating levels of maternal glucose, insulin, leptin, adiponectin, triglycerides, LDL-C, and HDL-C, and fetal insulin.
We included two studies of pregnant women from Oslo University Hospital, Norway: the prospective STORK (n = 263) and the cross-sectional 4-vessel method study (4-vessel; n = 165). We used multiple linear regression for data analyses. A non-linear BMI-PW association was observed, which leveled off from BMI25. Therefore, BMI <25 and ≥25 were analyzed separately (n = 170/122 and 93/43 for STORK/4-vessel). Confounding variables included maternal age, parity, and gestational age.
PW increased significantly per kg m only among BMI <25 (univariate model's std.β[p] = 0.233 [0.002] vs. 0.074[0.48]/0.296[0.001] vs. -0.030[0.85] for BMI <25 vs. ≥25 in STORK/4-vessel). Maternal early- but not late-pregnancy insulin and term fetal insulin were associated with PW. The estimated effect of early pregnancy insulin was similar between the BMI groups but statistically significant only among BMI <25 (std.β[p] = 0.182[0.016] vs. 0.203[0.07] for BMI <25 vs. ≥25). Late pregnancy leptin was inversely associated with PW with a 1.3/1.7-fold greater effect among BMI ≥25 than BMI <25 in the STORK/4-vessel.
The BMI-PW association was non-linear: an association was observed for BMI <25 but not for BMI ≥25. Leptin may be involved in the non-linear association through a placental-adipose tissue interplay. Maternal early pregnancy insulin and fetal insulin at term were associated with PW.
胎盘重量(PW)已被发现可介导母体 BMI 对胎儿大小的主要影响。尽管如此,BMI-PW 之间的关联仍未得到充分理解。因此,我们旨在探讨潜在的解释变量,包括妊娠体重增加(GWG)、孕早期和孕晚期母体内葡萄糖、胰岛素、瘦素、脂联素、甘油三酯、LDL-C 和 HDL-C 以及胎儿胰岛素的循环水平。
我们纳入了来自挪威奥斯陆大学医院的两项孕妇研究:前瞻性 STORK(n=263)和四血管法横断面研究(4-vessel;n=165)。我们使用多元线性回归进行数据分析。观察到 BMI-PW 之间存在非线性关联,从 BMI25 开始趋于平稳。因此,我们分别分析 BMI<25 和 BMI≥25(STORK/4-vessel 分别为 n=170/122 和 93/43)。混杂变量包括母亲年龄、产次和孕龄。
仅在 BMI<25 的情况下,PW 每公斤体重显著增加(单变量模型的标准β[p]分别为 0.233[0.002]和 0.074[0.48]/0.296[0.001],与 BMI<25 相比,0.030[0.85]对于 STORK/4-vessel 中的 BMI≥25)。母体内孕早期而非晚期胰岛素和足月胎儿胰岛素与 PW 相关。早孕期胰岛素的估计作用在 BMI 组之间相似,但仅在 BMI<25 时具有统计学意义(标准β[p]分别为 0.182[0.016]和 0.203[0.07],对于 BMI<25 与 BMI≥25 相比)。STORK/4-vessel 中,孕晚期瘦素与 PW 呈负相关,BMI≥25 时的效应比 BMI<25 时高 1.3/1.7 倍。
BMI-PW 之间的关联是非线性的:在 BMI<25 时存在关联,但在 BMI≥25 时不存在。瘦素可能通过胎盘-脂肪组织相互作用参与这种非线性关联。母体内孕早期胰岛素和足月胎儿胰岛素与 PW 相关。