Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice

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 m...

Full description

Saved in:
Bibliographic Details
Published in:Microbiome 2021-06, Vol.9 (1), p.1-145, Article 145
Main Authors: Zheng, Hong, Xu, Pengtao, Jiang, Qiaoying, Xu, Qingqing, Zheng, Yafei, Yan, Junjie, Ji, Hui, Ning, Jie, Zhang, Xi, Li, Chen, Zhang, Limin, Li, Yuping, Li, Xiaokun, Song, Weihong, Gao, Hongchang
Format: Article
Language:English
Subjects:
Acetate
Acetic acid
Antibiotics
Bacteria
Cognition
Cognitive ability
Diabetes
Diabetes mellitus (insulin dependent)
Fecal microflora
Glucose
Gut-brain axis
Hippocampus
Insulin
Intestinal microflora
Memory
Metabolome
Microbiome
Microbiomes
Microbiota
Phenotypes
Risk factors
Streptozocin
Synaptophysin
vagotomy
Vagus nerve
Vancomycin
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. Video Abstract
ISSN:2049-2618
2049-2618
DOI:10.1186/s40168-021-01088-9