Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
J Clin Lipidol. 2019 Sep-Oct;13(5):821-831. doi: 10.1016/j.jacl.2019.06.007. Epub 2019 Jun 29.
Fetal growth, an important predictor of cardiometabolic diseases in adults, is influenced by maternal and fetal genetic and environmental factors.
We investigated the association between maternal lipid genetic risk score (GRS) and fetal growth among 4 US racial-ethnic populations (Whites, Blacks, Hispanics, and Asians).
We extracted genotype data for 2008 pregnant women recruited in the National Institute of Child Health and Human Development Fetal Growth Studies-Singleton cohort with up to 6 standardized ultrasound examinations. GRS was calculated using 240 single-nucleotide polymorphisms previously associated with higher total cholesterol (GRS), low-density lipoprotein cholesterol (GRS), and triglycerides (GRS) and lower high-density lipoprotein cholesterol (GRS).
At 40 weeks' gestation, a unit increase in GRS was associated with 11.4 g higher fetal weight (95% confidence interval [CI] 2.8-20.0 g) among normal-weight Whites, 26.3 g (95% CI 6.0-46.6 g) among obese Blacks, and 30.8 g (95% CI 6.3-55.3 g) among obese Hispanics. Higher GRS was associated with increased fetal weight across 36 to 40 weeks among normal-weight Whites and across 13 to 20 weeks among normal-weight Asians, but with decreased fetal weight across 26 to 40 weeks among normal-weight Hispanics. Higher GRS was suggestively associated with increased fetal weight in males and decreased in females. Associations remained consistent after adjustment for serum lipids.
Associations between fetal weight and maternal lipid GRS appear to vary by maternal race-ethnic group, obesity status, and offspring sex. Genetic susceptibility to unfavorable lipid profiles contributes to fetal growth differences even among normal-weight women suggesting a potential future application in predicting aberrant fetal growth.
胎儿生长是成人患心血管代谢疾病的重要预测因素，受母婴遗传和环境因素的影响。
我们研究了美国 4 个人种群体（白种人、黑种人、西班牙裔和亚洲人）中母亲脂质遗传风险评分（GRS）与胎儿生长之间的关系。
我们从国立儿童健康与人类发展研究所胎儿生长研究-单胎队列中提取了 2008 名孕妇的基因型数据，这些孕妇接受了多达 6 次标准化超声检查。使用先前与总胆固醇（GRS）、低密度脂蛋白胆固醇（GRS）和甘油三酯（GRS）升高以及高密度脂蛋白胆固醇（GRS）降低相关的 240 个单核苷酸多态性计算 GRS。
在 40 周妊娠时，正常体重的白种人中，GRS 每增加 1 个单位，胎儿体重增加 11.4g（95%置信区间[CI] 2.8-20.0g）；肥胖的黑种人增加 26.3g（95% CI 6.0-46.6g）；肥胖的西班牙裔增加 30.8g（95% CI 6.3-55.3g）。在正常体重的白种人中，GRS 与 36 至 40 周期间胎儿体重增加有关，与正常体重的亚洲人 13 至 20 周期间胎儿体重增加有关，但与正常体重的西班牙裔人 26 至 40 周期间胎儿体重减少有关。GRS 较高与男性胎儿体重增加和女性胎儿体重减少有关。调整血清脂质后，这些关联仍然一致。
胎儿体重与母亲脂质 GRS 之间的关联似乎因母亲种族群体、肥胖状况和后代性别而异。对不良血脂谱的遗传易感性导致胎儿生长差异，即使在正常体重的女性中也是如此，这表明其在预测异常胎儿生长方面具有潜在的未来应用。
