ArticleNature communications2025
Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Prenatal targeted maternal pregnancy metabolomic profiles, child emotional and behavioral problems, and autism related traits in the NYU CHES cohort.Molecular psychiatry · 2026Article
- Tryptophan metabolism: A hidden regulator of female reproductive health beyond fertility.Chinese medical journal · 2026Review
- Maternal obesity induces macrophage to myofibroblast transition in kidneys of male offspring through a pathway driven by 20-hydroxyeicosatetraenoic acid.Nature communications · 2026Article
- PhenoAge acceleration, serum tryptophan, and frailty in socially engaged actively aging elderly men.iScience · 2026Article
- Modulation of the Kynurenine Pathway: A New Approach for Treating Neurodegeneration.Life (Basel, Switzerland) · 2026Review
- Cumulative environmental exposures adversely impact social behaviour and are associated with dysregulation of genes and proteins involved in epigenetic, ribosomal, and immune regulation in male mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Sex specific pattern of adipose expansion, inflammation and dysfunction with short term high fat diet exposure.Frontiers in endocrinology · 2026Article
- Tryptophan Metabolism in Neurodevelopment and Its Implications For Neurodevelopmental Disorders.Molecular neurobiology · 2025Review
- Impact of maternal microbiota imbalance during pregnancy on fetal cerebral neurodevelopment: Is there a link to certain autistic disorders?Brain, behavior, & immunity - health · 2025Review
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Authors and funding
9 authors.
Funding
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Abstract
Diet-related maternal obesity has been implicated in neurodevelopmental disorders in progeny. Although the precise mechanisms and effective interventions remain uncertain, our research elucidates some of these complexities. We established that a prenatal high-fat diet triggered maternal immune activation (MIA), marked by elevated serum lipopolysaccharide levels and inflammatory-cytokine overproduction, which dysregulated the maternal tryptophan metabolism promoting the accumulation of neurotoxic kynurenine metabolites in the embryonic brain. Interventions aimed at mitigating MIA or blocking the kynurenine pathway effectively rescued the male mice social performance. Furthermore, excessive kynurenine metabolites initiated oxidative stress response causing neuronal migration deficits in the fetal neocortex, an effect that was mitigated by administering the glutathione synthesis precursor N-Acetylcysteine, underscoring the central role of maternal immune-metabolic homeostasis in male mice behavioral outcomes. Collectively, our study accentuated the profound influence of maternal diet-induced immuno-metabolic dysregulation on fetal brain development and provided the preventive strategies for addressing neurodevelopmental disorders.
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