影响早产儿和足月新生儿脐带血浆瘦素和脂联素水平及其比值的母胎因素:胎儿代谢功能障碍起源的新见解

Precision nutrition Pub Date : 2022-11-01 Epub Date: 2022-08-18
Kartikeya Makker, Mingyu Zhang, Guoying Wang, Xiumei Hong, Khyzer B Aziz, Xiaobin Wang
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引用次数: 0

摘要

背景:了解影响出生时瘦素、脂联素和脂联素:瘦素比率的母体和胎儿因素,可能为潜在的未来代谢改变风险提供有价值的见解,并为原始预防和精确营养策略提供信息。目的:确定出生时影响瘦素和脂联素水平(肥胖的标志)和脂联素/瘦素比值(脂肪组织功能失调的标志)的母胎危险因素。方法:我们研究了波士顿出生队列中的母婴对。脐带血是在出生时采集的。我们使用学生t检验比较对数标准化脐带瘦素和脂联素水平。采用回归分析来检验母胎因素与足月和早产儿出生时瘦素和脂联素水平以及脂联素:瘦素比值的关系。结果:我们分析了1012名婴儿(245名早产儿)。足月儿脐带瘦素和脂联素均高于早产儿(分别为10.2±0.9比9.2±1.3,p < 0.0001和9.5±0.7比8.9±0.8,p < 0.0001)。黑人婴儿脐带瘦素较高(10.1±1.1 vs. 9.9±1.2;p < 0.001),尽管黑人(非黑人)婴儿脐带脂联素水平较低(9.3±0.8比9.5±0.7;P = 0.01)。脂联素与瘦素的比值(对数归一化)在早产儿中(-0.24)高于足月婴儿(-0.69)。经回归分析,脐带瘦素与较长胎龄、出生体重z分、黑人种族、母亲超重和肥胖、妊娠期糖尿病和妊娠期糖尿病呈正相关,与男性呈负相关。脐带脂联素与胎龄、出生体重z分呈正相关,与黑人、男性呈负相关。脂联素:瘦素比值与男性呈正相关,与GA、出生wt. z评分、黑人、妊娠期糖尿病、妊娠期糖尿病、母亲超重和肥胖呈负相关。结论:我们发现了几个影响瘦素和脂联素水平以及出生时脂联素-瘦素比值的因素,这些因素在影响这些激素的轨迹和未来的心脏代谢结果方面也起着重要作用。这些知识可以帮助量身定制精确的营养干预措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Maternal and fetal factors affecting cord plasma leptin and adiponectin levels and their ratio in preterm and term newborns: New insight on fetal origins of metabolic dysfunction.

Background: Understanding of maternal and fetal factors affecting leptin, adiponectin and adiponectin: leptin ratio at birth, may provide valuable insights into potential future risk of metabolic alterations and inform primordial prevention and precision nutrition strategies.

Objective: To identify maternal and fetal risk factors that affect leptin and adiponectin levels (markers of adiposity) and adiponectin/leptin ratio (a marker of dysfunctional adipose tissue) at birth.

Methods: We studied mother-infant pairs in the Boston Birth Cohort. Cord blood was collected at birth. We used student t-tests to compare log normalized cord leptin and adiponectin levels. Regression analysis were performed to examine the association of maternal and fetal factors with leptin and adiponectin levels and adiponectin: leptin ratio at birth in both term and preterm infants.

Results: We analyzed 1012 infants (245 preterm). Both cord leptin and adiponectin were higher in term infants than preterm infants (10.2 ± 0.9 vs. 9.2 ± 1.3, p < 0.0001 and 9.5 ± 0.7 vs. 8.9 ± 0.8, p < 0.0001 respectively). Cord leptin was higher for Black infants (10.1 ± 1.1 vs. 9.9 ± 1.2; p < 0.001) although Black (ref: non Black) infants had lower cord adiponectin levels (9.3 ± 0.8 vs. 9.5 ± 0.7; p = 0.01). Ratio of adiponectin to leptin (log normalized) was higher in preterm infants (-0.24) vs. term infants (-0.69). On regression analysis cord leptin was positively associated with longer gestational age, birth weight z score, Black race, maternal overweight and obesity, gestational diabetes and pregestational diabetes mellitus and negatively associated with male sex. Cord adiponectin was positively associated with gestational age, birth weight z score and negatively with Black race and male sex. Adiponectin: leptin ratio was positively with male sex and negatively with GA, birth wt. z score, Black race, gestational DM, pregestational DM and maternal overweight and obesity.

Conclusion: We identified several factors that affect leptin and adiponectin levels along with adiponectin-leptin ratio at birth beyond GA and birth weight which could also play an important role in influencing the trajectory of these hormones and future cardio metabolic outcomes. This knowledge can help tailor precision nutrition interventions.

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