Evidence map›Paper›PMID 42667471›Full record

ArticleMetabolic brain disease2026

Effects of imbalanced gut microbial on mice with type a hepatic encephalopathy through the gut-liver-brain axis.

Xiaoya Yang, Jiayuan Huang, Lei Wu, Tianyu Xu, Guoqiao Quan, Yuange Li, Tao Liu, Lingping Kong, Xingxiang He, Zhaoming Liu and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Xiaoya Yang *Department of Physiology, Guangzhou Health Science College, Guangzhou, China.
Jiayuan Huang *Department of Gastroenterology, The Eighth People's Hospital of Nanhai District, Foshan, China.
Lei Wu *Department of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Tianyu XuDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Guoqiao QuanDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Yuange LiDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Tao LiuDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Lingping KongDepartment of Physiology, Guangzhou Health Science College, Guangzhou, China.
Xingxiang HeDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Zhaoming LiuDepartment of Physiology, Guangzhou Health Science College, Guangzhou, China. liuzhaoming12@126.com.
Wenrui XieDepartment of Gastroenterology, Research Center for Engineering Techniques of Microbiota-Targeted Therapies of Guangdong Province, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China. wenruix@gdpu.edu.cn.

Funding

This study was supported by the Tertiary Education Scientific research project of Guangzhou Municipal Education Bureau (No. 202235423; No. 202032875), the China Postdoctoral Science Foundation (No. 2023M740782), and the Key-Area Research and Development Program of Guangdong Province (No. 2022B1111070006). No. 2022B1111070006
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe relationship between type A hepatic encephalopathy, a highly lethal disease, and gut microbiota remains unclear, and research on this topic is limited. The objective of our study was to investigate the correlation between an imbalance in the gut microbiota and type A hepatic encephalopathy and the impact of fecal microbiota transplantation.

methodsWe established a mouse model of gut microbiota disorder and type A hepatic encephalopathy. Feces from grades III and IV type A hepatic encephalopathy mice were transplanted into healthy mice. Antibiotic administration, intestinal symbiosis, and pathogenicity experiments were conducted. Behavioral, biochemical, pathological, 16 S rRNA gene amplicon sequencing analyses, and correlation analyses were performed.

resultsAntibiotic treatment caused a gut microbiota imbalance in mice. The degree of thioacetamide-induced type A hepatic encephalopathy was significantly aggravated after oral antibiotic administration, leading to a decline in the survival curve, accompanied by behavioral, biochemical, and pathological changes, as well as decreased Rikenellaceae levels. Transplanting feces from type A hepatic encephalopathy mice into healthy mice resulted in thioacetamide-like behavioral, biochemical, and tissue changes, as well as a significant decline in the abundance of the gut microbiota, an increase in the abundance of Prevotellaceae NK3B31, and a decrease in the abundance of Akkermansia muciniphila and Odoribacter. Additionally, significant correlations were observed between the abundances of the four intestinal microbial species and the majority of measured indicators in mice with type A hepatic encephalopathy. Notably, Akkermansia muciniphila exhibited particularly strong associations with these indicators. Although significant between-group differences were observed for Bacillus, Paenibacillus, Candidatus Saccharimonas, Escherichia-Shigella, UCG_002, Acinetobacter, and Proteus, no significant correlations were detected between these microbial taxa and any of the measured indicators.

conclusionsGut microbiota disorder aggravates lesions in thioacetamide-induced type A hepatic encephalopathy mice. Transplanting feces from mice with type A hepatic encephalopathy causes healthy mice to exhibit type A hepatic encephalopathy symptoms.

Indexed as

BrainBrain-Gut AxisDysbiosisGastrointestinal MicrobiomeHepatic EncephalopathyLiverAnimalsAnti-Bacterial AgentsDisease Models, AnimalFecal Microbiota TransplantationFecesMaleMiceMice, Inbred C57BLThioacetamideAnti-Bacterial AgentsThioacetamideAcute liver failureFecal microbiota transplantationGut-liver-brain axisHepatic encephalopathy

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.