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