母亲糖尿病和后代自闭症谱系障碍:流行病学证据和潜在生物学机制的综述

K. Bowers, Cuilin Zhang
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引用次数: 5

摘要

妊娠期糖尿病是一种常见的妊娠并发症,其在育龄妇女中的患病率正在上升,并对后代造成短期和长期的不良后果。妊娠期高血糖或其他不良的母体代谢特征可能通过几种潜在的介导机制(如炎症、氧化应激和表观遗传学)增加自闭症风险。本文综述了近年来有关母体妊娠前糖尿病、妊娠糖尿病、肥胖与后代自闭症谱系障碍(ASD)之间关系的研究进展。我们还将探索潜在的生物学机制来解释子宫内暴露于高血糖环境与ASD风险之间的关系,包括炎症、氧化应激和表观遗传学。考虑到妊娠期肥胖和糖尿病的同时增加,以及这些疾病的可改变性,它们与ASD的关联及其潜在的分子机制应进一步探讨。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Maternal Diabetes and Autism Spectrum Disorders in the Offspring: A Review of Epidemiological Evidence and Potential Biologic Mechanisms
Gestational diabetes is a common pregnancy complication whose prevalence is increasing among women of reproductive age and results in both short-and long-term adverse outcomes for the offspring.  Hyperglycemia or other consequences of adverse maternal metabolic profiles in pregnancy may contribute to autism risk through several potential mediating mechanisms, such as inflammation, oxidative stress, and epigenetics.  The present review aims to summarize recent studies exploring the association between maternal pre-gestational diabetes, gestational diabetes, obesity and autism spectrum disorders (ASD) in the offspring. We will also explore potential biologic mechanisms to explain the association between in utero exposure to a hyperglycemic environment and risk for ASD, including inflammation, oxidative stress and epigenetics.  Considering the concurrent rise in obesity and diabetes in pregnancy, as well as the modifiable nature of these disorders, their associations with ASD and the underlying molecular mechanisms should be explored further.
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