Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Department of Epidemiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
J Clin Endocrinol Metab. 2021 Apr 23;106(5):1427-1436. doi: 10.1210/clinem/dgab018.
Maternal oxidative stress in pregnancy can arise through a multitude of sources and may have lifelong consequences for the child. Animal studies suggest that prenatal oxidative stress may contribute to metabolic dysfunction and excessive weight gain in the offspring. However, this relationship has been studied minimally in humans.
Determine the association between prenatal oxidative stress biomarkers and child weight and body mass index (BMI) z-scores from birth to age 6.
Within The Infant Development and the Environment Study (TIDES) prospective pregnancy cohort, we calculated age- and sex-specific Z-scores for child weight and BMI, measured between birth and age 6 (N = 736). Three oxidative stress biomarkers were quantified in third-trimester urine, including 8-iso-prostaglandin F2α (8-iso-PGF2α), its primary metabolite, and prostaglandin F2α (PGF2α). We examined associations between each biomarker and Z-scores using linear regression as well as group-based trajectory modeling.
Prenatal 8-iso-PGF2α and its metabolite were associated with lower birth weight and higher weight at age 4. For example, an ln-unit increase in 8-iso-PGF2α was associated with 0.17 SD higher weight at age 4 (95% CI 0.01, 0.33). These biomarkers were also associated with higher BMI at age 4. Finally, within 4 unique weight trajectories (low, normal, high, and low-high), children of mothers with higher 8-iso-PGF2α were 2.56 times more likely (95% CI 1.22, 5.41) to be in the low-high trajectory than children in the normal group.
We observed associations between third-trimester oxidative stress and lower birth weight as well as higher early childhood weight and BMI. These findings have important implications for understanding the developmental origins of childhood weight gain and metabolic disease.
妊娠期间母体的氧化应激可能来自多种来源，并可能对儿童的一生造成影响。动物研究表明，产前氧化应激可能导致后代代谢功能障碍和体重过度增加。然而，这种关系在人类中研究甚少。
确定妊娠晚期氧化应激生物标志物与儿童出生至 6 岁时体重和体重指数（BMI）Z 评分之间的关系。
在婴儿发育与环境研究（TIDES）前瞻性妊娠队列中，我们计算了出生至 6 岁（N=736）期间儿童体重和 BMI 的年龄和性别特异性 Z 评分。在第三孕期尿液中定量测定了 3 种氧化应激生物标志物，包括 8-异前列腺素 F2α（8-iso-PGF2α）、其主要代谢产物和前列腺素 F2α（PGF2α）。我们使用线性回归和基于群组的轨迹建模来检查每个生物标志物与 Z 评分之间的关系。
产前 8-iso-PGF2α及其代谢产物与出生体重较低和 4 岁时体重较高有关。例如，ln 单位增加 8-iso-PGF2α与 4 岁时体重增加 0.17 个标准差（95%CI 0.01，0.33）有关。这些生物标志物也与 4 岁时的 BMI 较高有关。最后，在 4 种独特的体重轨迹（低、正常、高和低高）中，母亲 8-iso-PGF2α 较高的儿童成为低高轨迹的可能性是正常组儿童的 2.56 倍（95%CI 1.22，5.41）。
我们观察到妊娠晚期氧化应激与出生体重较低以及儿童早期体重和 BMI 较高之间存在关联。这些发现对于理解儿童体重增加和代谢疾病的发育起源具有重要意义。
