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The impact of gestational diabetes mellitus on fetal neural development: A systematic review.

PMID: 41791210 · DOI: 10.1016/j.braindev.2026.104521 · Brain & development, 2026 · Zenia Safwan, Emaan Ijaz, Hafsa Shamim, Arooj Fatima, Ashfaq Ahmad, Ahmed Murtaz Khalid
📄 Abstract

To synthesise existing research on the impact of gestational diabetes mellitus (GDM) on fetal neural development and subsequent cognitive function in offspring. A systematic review was conducted following PRISMA guidelines. PubMed, Cochrane Library, and ClinicalTrials.gov were searched from January 1964 to October 2024. Studies comparing offspring of mothers with GDM to those without were included. Quality was assessed using the Newcastle-Ottawa Scale (NOS). Seventeen studies met the inclusion criteria. The findings suggest that GDM is linked to subtle yet significant neurodevelopmental modifications, encompassing delays in communication and language proficiency, behavioural dysregulation, as well as heightened susceptibility to autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD). Electrophysiological investigations revealed alterations in cortical activity and extended auditory responses, while neuroimaging studies documented structural variations, including changes in the dimensions of the corpus callosum, ventricular size, and sulcal maturation. Molecular investigations uncovered dysregulated microRNAs that play a role in neurogenesis. Numerous studies emphasised the dose-dependent effects of maternal glucose concentrations and the protective impact of effective glycemic control. Maternal GDM is associated with alterations in fetal brain structure and function, which may predispose offspring to neurodevelopmental risks. While not all deficits persist, these findings highlight the potential value of early glycemic control and postnatal monitoring for at-risk infants. Further longitudinal research is needed to distinguish causal GDM effects from environmental confounders.

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Идентификация (6 полей)
Механизм действия (21 полей)
Mechanism
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Mutations (obesity/lean)
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Activity (obesity)
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Activity temporal
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Energy balance
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Appetite
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Fat metabolism
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Lipolysis
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Thermogenesis
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Muscle metabolism
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Inflammation
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Glucose metabolism
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AA metabolism
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Hormonal pathways
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Cell death
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Adipocyte fibrosis
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Upstream (biochem)
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Upstream (physiol)
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Экспрессия (8 полей)
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Клиника (11 полей)
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