题名 | Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice |
作者 | |
发表日期 | 2021-06-25 |
发表期刊 | MICROBIOME 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | Acetate Metabolome Diabetes Cognition Microbiome Gut-brain axis |
其他关键词 | SYNAPTIC VESICLE PROTEIN ; TYPE-1 ; SYNAPTOPHYSIN ; PERFORMANCE ; INFLAMMATION ; DYSFUNCTION ; DEMENTIA ; DATABASE ; DECLINE |
摘要 | Background: Modification of the gut microbiota has been reported to reduce the incidence of type 1 diabetes mellitus (T1D). We hypothesized that the gut microbiota shifts might also have an effect on cognitive functions in T1D. Herein we used a non-absorbable antibiotic vancomycin to modify the gut microbiota in streptozotocin (STZ)-induced T1D mice and studied the impact of microbial changes on cognitive performances in T1D mice and its potential gut-brain neural mechanism. Results: We found that vancomycin exposure disrupted the gut microbiome, altered host metabolic phenotypes, and facilitated cognitive impairment in T1D mice. Long-term acetate deficiency due to depletion of acetate-producing bacteria resulted in the reduction of synaptophysin (SYP) in the hippocampus as well as learning and memory impairments. Exogenous acetate supplement or fecal microbiota transplant recovered hippocampal SYP level in vancomycin-treated T1D mice, and this effect was attenuated by vagal inhibition or vagotomy. Conclusions: Our results demonstrate the protective role of microbiota metabolite acetate in cognitive functions and suggest long-term acetate deficiency as a risk factor of cognitive decline. |
资助项目 | National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [21974096, 22074106, 81771386]; Ten-thousand Talents Program of Zhejiang Province [2018R52052]; Qianjiang Talent Project of Zhejiang Province [QJD1802023]; National Key Research and Development Program [SQ2018YFE010015] |
出版者 | BMC |
出版地 | LONDON |
ISSN | 2049-2618 |
卷号 | 9期号:1页码:145 |
DOI | 10.1186/s40168-021-01088-9 |
页数 | 19 |
WOS类目 | Microbiology |
WOS研究方向 | Microbiology |
WOS记录号 | WOS:000668588700002 |
收录类别 | SCIE ; PUBMED ; SCOPUS |
URL | 查看原文 |
PubMed ID | 34172092 |
PMC记录号 | PMC8235853 |
SCOPUSEID | 2-s2.0-85111473108 |
自科自定义期刊分类 | T3(A)类 |
通讯作者地址 | [Gao, Hongchang]Institute of Aging,School of Mental Health,Wenzhou Medical University,Wenzhou,325035,China ; [Song, Weihong]Institute of Aging,School of Mental Health,Wenzhou Medical University,Wenzhou,325035,China |
Scopus学科分类 | Microbiology;Microbiology (medical) |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/6078 |
专题 | 附属第二医院_核磁共振室 药学院(分析测试中心) 附属第一医院 精神医学学院 第一临床医学院(信息与工程学院)、附属第一医院_内科学_呼吸与危重症医学科 |
通讯作者 | Song, Weihong; Gao, Hongchang |
作者单位 | 1.Institute of Metabonomics & Medical NMR,School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,325035,China; 2.Department of Pulmonary and Critical Care Medicine,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325015,China; 3.Institute of Aging,School of Mental Health,Wenzhou Medical University,Wenzhou,325035,China; 4.State Key Laboratory of Magnetic Resonance and Atomic and Molecular Physics,Wuhan Institute of Physics and Mathematics,Chinese Academy of Sciences,Wuhan,430070,China |
第一作者单位 | 药学院(分析测试中心); 附属第一医院; 第一临床医学院(信息与工程学院)、附属第一医院; 精神医学学院 |
通讯作者单位 | 精神医学学院 |
第一作者的第一单位 | 药学院(分析测试中心) |
推荐引用方式 GB/T 7714 | Zheng, Hong,Xu, Pengtao,Jiang, Qiaoying,et al. Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice[J]. MICROBIOME,2021,9(1):145. |
APA | Zheng, Hong., Xu, Pengtao., Jiang, Qiaoying., Xu, Qingqing., Zheng, Yafei., ... & Gao, Hongchang. (2021). Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice. MICROBIOME, 9(1), 145. |
MLA | Zheng, Hong,et al."Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice".MICROBIOME 9.1(2021):145. |
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