Department of Psychiatry, Oregon Health & Science University, United States; Center for Mental Health Innovation, Oregon Health & Science University, United States; Division of Neuroscience, Oregon National Primary Research Center, United States.
Department of Psychiatry, Oregon Health & Science University, United States; Center for Mental Health Innovation, Oregon Health & Science University, United States.
Brain Behav Immun. 2024 Aug;120:34-43. doi: 10.1016/j.bbi.2024.05.018. Epub 2024 May 19.
Increased adiposity during pregnancy may be related to offspring risk for mental health disorders, although the biological mechanisms are poorly understood. One promising hypothesis is that factors secreted from adipocytes such as leptin and adiponectin may explain this association. The current study examined whether pregnancy or umbilical cord blood concentrations of leptin and/or adiponectin a) predict elevated infant negative affect at 6 months (an early life marker of risk for psychopathology); and b) help explain the association between pregnancy adiposity and increased infant negative affect.
Data came from a prospective cohort (N = 305) of pregnant individuals and their offspring. Second trimester adiposity was assessed using air displacement plethysmography. Concentrations of leptin and adiponectin were measured in second trimester plasma and umbilical cord plasma. Infant negative affect was assessed by standardized observation at 6 months. Second trimester inflammation was assessed using a comprehensive panel of cytokines.
Lower second trimester adiponectin was associated with elevated infant negative affect, and mediated the effect of pregnancy adiposity on infant negative affect. This association was independent of the effect of second trimester inflammation. Umbilical cord leptin also predicted higher infant negative affect and mediated the association between pregnancy adiposity and infant negative affect.
This is the first study to link pregnancy adiponectin or cord blood leptin to infant markers of risk for psychopathology, and the first to demonstrate that these adipokines mediate the association between pregnancy adiposity and offspring behavioral outcomes, suggesting novel markers of risk and potential mechanisms of effect.
孕期脂肪增加可能与后代心理健康障碍的风险有关,尽管其生物学机制尚不清楚。一个有前途的假设是,脂肪细胞分泌的因子,如瘦素和脂联素,可能解释这种关联。本研究旨在检验孕妇和脐血中瘦素和/或脂联素水平:a)是否可预测婴儿 6 个月时的负面情绪升高(这是精神病理学风险的早期生命标志物);b)是否有助于解释孕期肥胖与婴儿负面情绪增加之间的关联。
本研究的数据来自一个前瞻性队列(N=305),包括孕妇及其后代。通过空气置换体描仪评估孕中期的肥胖程度。采用酶联免疫吸附试验法测量孕中期和脐血中瘦素和脂联素的浓度。采用标准化观察法评估婴儿 6 个月时的负面情绪。采用细胞因子综合面板评估孕中期炎症。
孕中期脂联素水平较低与婴儿负面情绪升高有关,并介导了孕期肥胖对婴儿负面情绪的影响。这种关联独立于孕中期炎症的影响。脐血瘦素也预测婴儿负面情绪较高,并介导了孕期肥胖与婴儿负面情绪之间的关联。
这是首次将孕期脂联素或脐血瘦素与婴儿精神病理学风险标志物联系起来的研究,也是首次表明这些脂肪因子介导了孕期肥胖与后代行为结果之间的关联,为风险标志物提供了新的认识,并为潜在的作用机制提供了新的认识。