Association of Gestational Diabetes Mellitus Complicated With Short Sleep Duration and Child Neurodevelopmental Delay
妊娠期糖尿病合并睡眠时间短与儿童神经发育迟缓的关系
Authors: Zhu Y, Wang H, Ma R, Zhang L, Wang Y, Zhang Y, Shao Z, Zhu D, Zhu P.
Source:The Journal of Clinical Endocrinology & Metabolism, Volume 109, Issue 1, January 2024, Pages e216–e224
Gestational diabetes mellitus (GDM) is a risk factor for child neurodevelopmental delay. Maternal short sleep duration (SSD) may aggravate glucose metabolism disorder in women with GDM. However, it is unclear whether maternal SSD will further affect the neurodevelopmental outcomes of children.
To identify the association of GDM complicated with SSD and child neurodevelopmental delay.
This prospective study included 7069 mother-child pairs. Between 24 and 28 weeks of gestation, GDM was based on the 75-g oral-glucose-tolerance test. Self-reported sleep duration was collected via the Pittsburgh Sleep Quality Index questionnaire in the second (24-28 weeks) and third (32-36 weeks) trimesters. Outcomes of neurodevelopmental delay in 6 to 36 months postpartum were evaluated using Denver Developmental Screening Test-II and Gesell Development Diagnosis Scale.
Compared with the unexposed group, women with “GDM + SSD” have the greatest risks of child neurodevelopmental delay (hazard ratio with 95% CI: 1.58 [1.03-2.44]). “GDM + SSD” was associated with the greatest risks of maternal-fetal glucose metabolic disorder. An interquartile ratio (0.58 mmol/L) increase in cord blood C-peptide was associated with the risk of child neurodevelopmental delay (hazard ratio with 95% CI: 1.28 [1.12-1.48]). The stronger linear association of maternal glucose metabolism profiles and C-peptide in women with “GDM + SSD” was also demonstrated. The proportion of association between “GDM + SSD” and child neurodevelopmental delay mediated by C-peptide was 14.4%.
GDM complicated with SSD was associated with increased risk for child neurodevelopmental delay by enhancing the intergenerational association of maternal-fetal glucose metabolism disorder.
摘要
妊娠期糖尿病(GDM)是儿童神经发育迟缓的危险因素。孕产妇睡眠时间短 (SSD) 可能会加重 GDM 女性的葡萄糖代谢紊乱。然而,目前尚不清楚母体SSD是否会进一步影响儿童的神经发育结局。
确定GDM并发SSD与儿童神经发育迟缓的关联。
这项前瞻性研究包括 7069 对母子。在妊娠 24 至 28 周之间,GDM 基于 75 g 口服葡萄糖耐量试验。在第二个(24-28 周)和第三个(32-36 周)三个月通过匹兹堡睡眠质量指数问卷收集自我报告的睡眠持续时间。使用丹佛发育筛查试验 II 和 Gesell 发育诊断量表评估产后 6 至 36 个月神经发育迟缓的结果。
与未暴露组相比,“GDM+SSD”女性发生儿童神经发育迟缓的风险最大(95%CI的风险比:1.58 [1.03-2.44])。“GDM+SSD”与母胎葡萄糖代谢紊乱风险最大相关。脐带血C肽的四分位数比值(0.58mmol/L)与儿童神经发育迟缓的风险相关(95%CI的风险比:1.28 [1.12-1.48])。还证明了母体葡萄糖代谢谱和 C 肽与“GDM + SSD”的更强线性关联。“GDM+SSD”与C肽介导的儿童神经发育迟缓的关联比例为14.4%。
GDM合并SSD通过增强母胎葡萄糖代谢紊乱的代际关联,与儿童神经发育迟缓风险增加相关。
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