Evidence map›Paper›PMID 40506791›Full record

ArticleBehavioral and brain functions : BBF2025

The gut microbiome and metabolomic alterations underlying colitis-induced encephalopathy in mice: mechanistic insight.

Aimin Cai, Dingchao Shen, Qiushuang Xiong, Shize Li, Chenyu Qiu, Lele Li, Zhiwei Chen, Xinlu Lin, Qing Yao, Youting Zhang and 2 more

Abstract read
In one paragraph

Article in Behavioral and brain functions : BBF, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Aimin Cai *Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Dingchao Shen *Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Qiushuang Xiong *Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Shize LiWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Chenyu QiuWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Lele LiWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Zhiwei ChenWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Xinlu LinWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Qing YaoWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Youting ZhangWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. zytwzyxy@163.com.
Ruijie ChenWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. crjpharm@163.com.
Longfa KouWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China. klfpharm@163.com.

Funding

Wenzhou Science and Technology Bureau Y20210133Zhejiang Medical and Health Science and Technology Program 2023KY907Zhejiang Medical Association Clinical Medical Research special fund project 2024ZYC-A10
6 · The paper itself

Abstract

backgroundIn addition to classical gastrointestinal symptoms, patients with inflammatory bowel disease (IBD) often exhibit neurological manifestations, such as mood disorders and cognitive dysfunctions, which are frequently overlooked. However, the potential pathogenesis of IBD-related encephalopathy remains unclear, and few studies have explored the influence of interactions between the gut microbiota and the host gut-brain metabolome on the emergence of brain diseases in IBD mice. In this study, we conducted a comprehensive analysis of gut microbiome and metabolome alterations in dextran sulfate sodium salt (DSS)-induced IBD mice compared to control mice, focusing on colonic contents and hippocampal tissue. Our aim was to investigate the putative mechanisms underlying the microbiota-gut-brain axis in IBD-induced encephalopathy.

resultsIBD mice showed depression-like behaviors and cognitive deficits. Metabolic profiling revealed distinct patterns in the colonic contents and hippocampal areas of IBD mice, marked by decreased energy metabolism, amino acid levels, short-chain fatty acids (SCFAs), and choline metabolism. These metabolic changes were negatively associated with the abundance of Bacteroides, Turicibacter, Ruminococcus, and Akkermansia, while Desulfovibrio and Lactobacillus showed positive correlations.

conclusionsThis study identifies unique microbial and gut-brain metabolite signatures associated with DSS-induced changes and offers new metabolic insights into the microbiota-gut-brain axis in IBD-related brain disorders. It highlights the potential of targeting gut microbiota to modulate host metabolism as a therapeutic approach for IBD-related neurological complications.

Indexed as

Brain DiseasesColitisGastrointestinal MicrobiomeInflammatory Bowel DiseasesMetabolomeAnimalsBrainBrain-Gut AxisColonDextran SulfateDisease Models, AnimalFatty Acids, VolatileHippocampusMaleMetabolomicsMiceDextran SulfateFatty Acids, VolatileCognitive dysfunctionsDSS-induced colitisMetabolismMicrobiota-gut-brain axisMood disorders

Identifiers

PMID40506791
PMCPMC12160427

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.