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高纤维饮食通过肠道-大脑轴减轻母源性肥胖引起的后代认知和社交功能障碍。

High-fiber diet mitigates maternal obesity-induced cognitive and social dysfunction in the offspring via gut-brain axis.

机构信息

College of Food Science and Engineering, Northwest A&F University, Yangling 712100, Shaanxi, China.

BGI Institute of Applied Agriculture, BGI-Shenzhen, Shenzhen 518120, Guangdong, China.

出版信息

Cell Metab. 2021 May 4;33(5):923-938.e6. doi: 10.1016/j.cmet.2021.02.002. Epub 2021 Mar 1.

DOI:10.1016/j.cmet.2021.02.002
PMID:33651981
Abstract

Maternal obesity has been reported to be related to neurodevelopmental disorders in the offspring. However, the underlying mechanisms and effective interventions remain unclear. This cross-sectional study with 778 children aged 7-14 years in China indicated that maternal obesity is strongly associated with children's lower cognition and sociality. Moreover, it has been demonstrated that maternal obesity in mice disrupted the behavior and gut microbiome in offspring, both of which were restored by a high-fiber diet in either dams or offspring via alleviating synaptic impairments and microglial maturation defects. Co-housing and feces microbiota transplantation experiments revealed a causal relationship between microbiota and behavioral changes. Moreover, treatment with the microbiota-derived short-chain fatty acids also alleviated the behavioral deficits in the offspring of obese dams. Together, our study indicated that the microbiota-metabolites-brain axis may underlie maternal obesity-induced cognitive and social dysfunctions and that high dietary fiber intake could be a promising intervention.

摘要

母亲肥胖与后代神经发育障碍有关。然而,潜在机制和有效干预措施仍不清楚。本项在中国 778 名 7-14 岁儿童中开展的横断面研究表明,母亲肥胖与儿童认知和社会性降低显著相关。此外,研究显示,肥胖母亲的小鼠后代表现出行为和肠道微生物组紊乱,而通过母鼠或子代高纤维饮食干预,可通过减轻突触损伤和小胶质细胞成熟缺陷来恢复这些紊乱。共笼和粪便微生物组移植实验揭示了微生物组和行为变化之间的因果关系。此外,用源自微生物组的短链脂肪酸进行治疗也可以缓解肥胖母鼠后代的行为缺陷。综上,本研究表明,微生物组-代谢物-脑轴可能是母亲肥胖导致认知和社交功能障碍的基础,而高膳食纤维摄入可能是一种有前景的干预措施。

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