Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice

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 imm...

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Main Authors: Penghao Sun, Mengli Wang, Xuejun Chai, Yong-Xin Liu, Luqi Li, Wei Zheng, Shulin Chen, Xiaoyan Zhu, Shanting Zhao
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-57414-4
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author Penghao Sun
Mengli Wang
Xuejun Chai
Yong-Xin Liu
Luqi Li
Wei Zheng
Shulin Chen
Xiaoyan Zhu
Shanting Zhao
author_facet Penghao Sun
Mengli Wang
Xuejun Chai
Yong-Xin Liu
Luqi Li
Wei Zheng
Shulin Chen
Xiaoyan Zhu
Shanting Zhao
author_sort Penghao Sun
collection DOAJ
description 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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issn 2041-1723
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publisher Nature Portfolio
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spelling doaj-art-29e427dd1d684a75a1ace33ad25fbb382025-08-20T02:01:30ZengNature PortfolioNature Communications2041-17232025-03-0116111810.1038/s41467-025-57414-4Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male micePenghao Sun0Mengli Wang1Xuejun Chai2Yong-Xin Liu3Luqi Li4Wei Zheng5Shulin Chen6Xiaoyan Zhu7Shanting Zhao8College of Veterinary Medicine, Northwest A&F UniversityCollege of Veterinary Medicine, Northwest A&F UniversityCollege of Basic Medicine, Xi’an Medical UniversityShenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Genome Analysis Laboratory of the Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural SciencesLife Science Research Core Services, Northwest A&F UniversityCollege of Resources and Environment Sciences, Northwest A&F UniversityCollege of Veterinary Medicine, Northwest A&F UniversityCollege of Veterinary Medicine, Northwest A&F UniversityCollege of Veterinary Medicine, Northwest A&F UniversityAbstract 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.https://doi.org/10.1038/s41467-025-57414-4
spellingShingle Penghao Sun
Mengli Wang
Xuejun Chai
Yong-Xin Liu
Luqi Li
Wei Zheng
Shulin Chen
Xiaoyan Zhu
Shanting Zhao
Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
Nature Communications
title Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
title_full Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
title_fullStr Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
title_full_unstemmed Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
title_short Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice
title_sort disruption of tryptophan metabolism by high fat diet triggered maternal immune activation promotes social behavioral deficits in male mice
url https://doi.org/10.1038/s41467-025-57414-4
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