Division of Chronic Disease Research Across the Lifecourse (CoRAL), Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA.
Duke-NUS Graduate Medical School, Singapore.
Int J Obes (Lond). 2018 Apr;42(4):608-617. doi: 10.1038/ijo.2017.256. Epub 2017 Oct 13.
Higher leptin and lower adiponectin correlate with adult and childhood adiposity, but it is unclear how exposure to these adipokines during gestation relates to offspring growth. We aimed to investigate the relationships of maternal and cord adipokines with offspring adiposity across childhood to early adolescence, as well as interactions with child age.
In mother-child pairs in the Project Viva cohort, we measured adipokines in mothers at second trimester (n=1106) and in cord blood at birth (n=657). We measured offspring adiposity indices at early childhood (mean 3.3±s.d. 0.3 years), mid-childhood (7.9±0.8 years) and early adolescence (13.2±0.9 years). We analyzed associations of maternal and cord adipokines with offspring longitudinal adiposity using a linear mixed model adjusting for pre-pregnancy body mass index (BMI), gestational weight gain (GWG), and other confounders.
Mothers with higher BMI and GWG had higher leptin. Offspring born to mothers with the highest vs lowest quartile of leptin had lower BMI z-score (-0.49 units, 95% confidence interval (CI):-0.72,-0.26), waist circumference (-2.6 cm, 95% CI: -3.7,-1.5) and sum of subscapular and triceps skinfolds (-2.8 mm, 95% CI: -4.1,-1.4) in early life. An interaction term between maternal leptin and child age was positive, suggesting that the associations between maternal leptin and child adiposity were not constant over time. Offspring born to mothers with lowest vs highest quartile of maternal adiponectin had lower early life adiposity (BMI z-score -0.27 units, 95% CI: -0.48,-0.05). Results were similar for cord leptin but not cord adiponectin.
Our findings showed higher maternal and cord leptin, and lower maternal adiponectin are associated with lower offspring adiposity from childhood to early adolescence, independent of maternal BMI and GWG. However, the strength of these associations was not constant over time.
瘦素和脂联素水平较高与成人和儿童肥胖相关,但孕期接触这些脂肪因子与后代生长的关系尚不清楚。本研究旨在探讨母亲和脐带脂肪因子与儿童期至青春期早期的后代肥胖相关,并探讨其与儿童年龄的相互作用。
在 Viva 项目的母婴队列中,我们在妊娠中期(n=1106)和出生时(n=657)测量了母亲和脐带的脂肪因子。我们在儿童早期(平均 3.3±0.3 岁)、中期(7.9±0.8 岁)和青春期早期(13.2±0.9 岁)测量了后代的肥胖指数。我们使用线性混合模型,在调整了孕前体重指数(BMI)、妊娠增重(GWG)和其他混杂因素后,分析了母亲和脐带脂肪因子与后代纵向肥胖的相关性。
BMI 和 GWG 较高的母亲瘦素水平较高。与瘦素最低四分位数相比,母亲瘦素最高四分位数的后代 BMI z 评分(-0.49 单位,95%置信区间(CI):-0.72,-0.26)、腰围(-2.6cm,95% CI:-3.7,-1.5)和肩胛下和肱三头肌皮褶厚度总和(-2.8mm,95% CI:-4.1,-1.4)较低。母亲瘦素与儿童年龄的交互项为正,表明母亲瘦素与儿童肥胖的相关性并非随时间恒定不变。与母亲瘦素最高四分位数相比,母亲瘦素最低四分位数的后代在儿童早期的肥胖程度较低(BMI z 评分-0.27 单位,95% CI:-0.48,-0.05)。脐带瘦素的结果与之相似,但脐带脂联素的结果则不然。
本研究结果表明,较高的母血和脐血瘦素以及较低的母血脂联素与儿童期至青春期早期的后代肥胖呈负相关,与母亲 BMI 和 GWG 无关。然而,这些关联的强度并非随时间恒定不变。