INSERM, U1018, Center for Research in Epidemiology and Population Health, Lifelong Epidemiology of Diabetes, Obesity, and Chronic Kidney Disease, Villejuif, France.
Diabetes. 2011 Aug;60(8):2152-9. doi: 10.2337/db10-1189. Epub 2011 Jun 23.
To understand the relationships between maternal glycemia during pregnancy and prenatal and early postnatal growth by evaluating cord C-peptide and IGF-I as mediating biomarkers in boys and girls separately.
We evaluated 342 neonates within the EDEN mother-child cohort study born to mothers without diabetes diagnosis before pregnancy. We measured maternal glycemia at 24-28 weeks of gestation and neonates' cord blood C-peptide (used as a proxy for fetal insulin) and IGF-I at birth. Reported maternal prepregnancy BMI and all measured infant weights and lengths in the 1st year were recorded. Growth modeling was used to obtain an individual growth curve for each infant in the 1st year. Path models, a type of structural equation modeling, were used for statistical analysis. Path analysis is a multivariate method associated with a graphical display that allows evaluation of mediating factors and distinguishes direct, indirect, and total effects.
Cord C-peptide at birth was positively correlated with maternal prepregnancy BMI and maternal glycemia and was higher in girls. In a path model that represented prenatal growth, there was no significant direct effect of maternal glycemia on birth weight, but the effect of maternal glycemia on birth weight was mediated by fetal insulin and IGF-I in both girls and boys. However, in girls only, higher concentrations of cord C-peptide (but not cord IGF-I or maternal glucose) were associated with slower weight growth in the first 3 months of life.
Our study underlines the role of the fetal insulin-IGF-I axis in the relationship between maternal glycemia during pregnancy and birth weight. We also show for the first time that high insulin concentration in female fetuses is associated with slower early postnatal growth. This slow, early growth pattern may be programmed by fetal hyperinsulinemia, and girls may be more susceptible than boys to its consequences.
通过评估脐带 C 肽和 IGF-I 作为中介生物标志物，分别在男孩和女孩中研究妊娠期间母体血糖与产前和产后早期生长的关系。
我们评估了 EDEN 母婴队列研究中的 342 名新生儿，这些新生儿的母亲在怀孕前没有糖尿病诊断。我们测量了妊娠 24-28 周时的母体血糖，以及新生儿出生时的脐带血 C 肽（用作胎儿胰岛素的替代物）和 IGF-I。记录了报告的母亲孕前 BMI 以及婴儿在第 1 年中所有测量的体重和长度。生长模型用于获得每个婴儿在第 1 年的个体生长曲线。路径模型（一种结构方程模型）用于统计分析。路径分析是一种与图形显示相关联的多元方法，允许评估中介因素，并区分直接、间接和总效应。
出生时的脐带 C 肽与母亲的孕前 BMI 和母体血糖呈正相关，且在女孩中更高。在一个代表产前生长的路径模型中，母体血糖对出生体重没有显著的直接影响，但母体血糖对出生体重的影响在女孩和男孩中均通过胎儿胰岛素和 IGF-I 介导。然而，仅在女孩中，较高浓度的脐带 C 肽（而不是脐带 IGF-I 或母体葡萄糖）与生命最初 3 个月体重增长缓慢有关。
我们的研究强调了胎儿胰岛素-IGF-I 轴在妊娠期间母体血糖与出生体重之间关系中的作用。我们还首次表明，女性胎儿中较高的胰岛素浓度与产后早期生长较慢有关。这种缓慢的早期生长模式可能是由胎儿高胰岛素血症编程的，而女孩比男孩更容易受到其后果的影响。
