{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zheng H"],"funding":["Qianjiang Talent Project of Zhejiang Province","National Natural Science Foundation of China","National Key Research and Development Program","Ten-thousand Talents Program of Zhejiang Province"],"pagination":["145"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8235853"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["<h4>Background</h4>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.<h4>Results</h4>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 we"],"journal":["Microbiome"],"pubmed_title":["Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice."],"pmcid":["PMC8235853"],"funding_grant_id":["22074106","2018R52052","81771386","SQ2018YFE010015","21974096","QJD1802023"],"pubmed_authors":["Zheng Y","Yan J","Xu P","Ji H","Li C","Xu Q","Jiang Q","Ning J","Zhang L","Gao H","Li X","Li Y","Zheng H","Zhang X","Song W"],"additional_accession":[]},"is_claimable":false,"name":"Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice.","description":"<h4>Background</h4>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.<h4>Results</h4>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 we","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-07-16T13:55:49.415Z","creation":"2022-02-11T00:29:29.217Z"},"accession":"S-EPMC8235853","cross_references":{"pubmed":["34172092"],"doi":["10.1186/s40168-021-01088-9"]}}