Evidence map›Paper›PMID 41299593›Full record

ArticleBMC medicine2025

Gut microbial tyramine facilitates intestinal damage and metabolic dysfunction-associated steatotic liver disease development.

Jia Wei, Shuangquan Liu, Jiayou Luo, Fei Yang, Wen Dai, Zhihang Huang, Xiongfeng Pan, Miyang Luo

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In one paragraph

Article in BMC medicine, 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
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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

8 authors.

Jia Wei *Department of Clinical Laboratory Medicine, Institution of Microbiology and Infectious Diseases, Hunan Province Clinical Research Center for Accurate Diagnosis and Treatment of High-incidence Sexually Transmitted Diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China.
Shuangquan Liu *Department of Clinical Laboratory Medicine, Institution of Microbiology and Infectious Diseases, Hunan Province Clinical Research Center for Accurate Diagnosis and Treatment of High-incidence Sexually Transmitted Diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China.
Jiayou LuoHunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China.
Fei YangHunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang, China.
Wen DaiHunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China.
Zhihang HuangHunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China.
Xiongfeng PanPediatrics Research Institute of Hunan Province, Hunan Children's Hospital, Changsha, China.
Miyang LuoHunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China. miyangluo@csu.edu.cn.

Funding

the Hunan Province Natural Science Foundation 2022JJ40668the National Natural Science Foundation of China 82304171
6 · The paper itself

Abstract

backgroundEmerging evidence indicates that gut microbiota and intestinal injury are crucial in pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), yet the role of key gut microbial metabolites such as tyramine in pediatric MASLD remains largely unknown. In this study, we aimed to explore the role of gut microbial tyramine in intestinal damage and MASLD development in children.

methodsWe investigated the functions and mechanisms of previously isolated Enterococcus faecium B6 (E. faecium B6) and its derived tyramine in a mice model of intestinal injury and MASLD development. An integrative analysis of transcriptomics and proteomics was performed on mouse liver to explore the molecular mechanisms of tyramine in MASLD progression. Targeted metabolomics was performed using fecal samples from a hospital-based population (27 MASLD cases and 27 matched controls) to measure tyramine levels. The association of serum tyramine and MASLD risk was then validated in a school-based population, using serum samples of 294 children in the MASLD group and 235 controls.

resultsE. faecium B6 and its metabolite tyramine significantly disrupted the intestinal barrier and increased intestinal permeability in mice. Tyramine supplementation promoted MASLD-related metabolic phenotype in mice. Multi-omics analysis indicated that the PPAR signaling pathway played an important role in the molecular mechanisms. Tyramine contributed to lipid accumulation mainly by increasing lipid synthesis and lipid uptake but reducing the β-oxidation processes in the mouse liver, as shown by real-time quantitative polymerase chain reaction and western blot. Furthermore, we demonstrated from the hospital-based cohort that tyramine concentration was significantly higher in the MASLD group than in the control group. Consistently, the school-based cohort demonstrated a higher risk of MASLD in the high-tyramine group compared to the low-tyramine group, with adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of 3.65 (95% CI: 2.66-4.32).

conclusionsThese results demonstrated that gut microbial tyramine effectively induced intestinal damage and facilitated MASLD development in mice. Tyramine was positively associated with the risk of MASLD in children. This study offered mechanistic insights into the pathogenesis of MASLD and opened therapeutic opportunities for such metabolic diseases.

Indexed as

Fatty LiverGastrointestinal MicrobiomeIntestinesTyramineAnimalsCase-Control StudiesChildDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLTyramineIntestinal damageLipid metabolismMASLDMetaboliteTyramine

Identifiers

PMID41299593
PMCPMC12659070

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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.