怀孕期间母亲皮质醇与婴儿肥胖:一项前瞻性调查

S. Entringer, C. Buss, J. Rasmussen, K. Lindsay, D. Gillen, D. Cooper, P. Wadhwa
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引用次数: 32

摘要

糖皮质激素在子宫内细胞生长和分化过程中起着关键作用。有证据表明,在敏感的发育时期暴露于不适当浓度的糖皮质激素可能会产生影响肥胖风险的生理系统改变。目的探讨妊娠期母亲皮质醇浓度与婴儿肥胖的相关性。设计、参与者和环境在南加州的大学产科诊所招募了67对早期妊娠的母子,并对其进行了从妊娠早期到分娩直到产后6个月的一系列评估。在妊娠早期(= 13周)、中期(= 24周)和妊娠晚期(= 30周)连续4天评估母体累积皮质醇生成(5份唾液样本/d × 4天× 3个月= 60份唾液样本/受试者)。在新生儿(出生后25天)和6个月大时,用双能x线吸收仪成像对婴儿身体组成进行了连续评估。结果在调整了关键的产前、出生和产后协变量后,妊娠晚期早期较高的母亲皮质醇(以先前的妊娠早期和妊娠中期皮质醇浓度为条件)与婴儿1至6个月大的体脂百分比变化显著相关[部分r(经协变量调整)= 0.379,P = 0.007],占儿童肥胖风险测量方差的约14%。结论本研究结果提示母体皮质醇对婴儿产后早期肥胖增加具有妊娠期特异性作用,并为人类提供证据,支持糖皮质激素在儿童肥胖风险的胎儿规划中的作用。
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Maternal Cortisol During Pregnancy and Infant Adiposity: A Prospective Investigation
Context Glucocorticoids play a key role during intrauterine development in cellular growth and differentiation. Evidence suggests that exposure to inappropriate concentrations of glucocorticoids during sensitive developmental periods may produce alterations in physiological systems that impact obesity risk. Objective To elucidate the magnitude and stage-of-gestation-specific association of maternal cortisol concentrations during pregnancy with infant adiposity. Design, Participants, and Setting Sixty-seven mother-child dyads recruited in early pregnancy at university-based obstetric clinics in Southern California were followed with serial assessments from early gestation through birth until 6 months postnatal age. Maternal cumulative cortisol production was assessed over each of 4 consecutive days in early (≅13 weeks), mid (≅24 weeks), and late pregnancy (≅30 weeks) (5 saliva samples/d × 4 days × 3 trimesters = 60 saliva samples/subject). Infant body composition was serially assessed in newborns (at ∼25 days postnatal age) and at ∼6 months age with dual-energy X-ray absorptiometry imaging. Results After adjusting for key prenatal, birth, and postnatal covariates, higher maternal cortisol during the early third trimester (conditioned on prior early and midgestation cortisol concentrations) was significantly associated with a greater change in infant percent body fat from 1 to 6 months of age [partial r (adjusted for covariates) = 0.379, P = 0.007], accounting for ∼14% of the variance in this measure of childhood obesity risk. Conclusion The present findings suggest a stage-of-gestation-specific effect of maternal cortisol on infant adiposity gain in early postnatal life and provide evidence in humans to support the role of glucocorticoids in fetal programming of childhood obesity risk.
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