Altered oral microbiome and metabolites are associated with improved lipid metabolism in HBV-infected patients with metabolic dysfunction-associated fatty liver disease.
10.12122/j.issn.1673-4254.2025.09.23
- Author:
Jingjing ZHANG
1
;
Song FENG
2
;
Dali ZHANG
1
;
Jian XUE
3
;
Chao ZHOU
1
;
Pengcheng LIU
1
;
Shuangnan FU
1
;
Man GONG
1
;
Hui FENG
2
;
Ning ZHANG
1
Author Information
1. Senior Department of Hepatology, Chinese PLA General Hospital, Beijing 100039, China.
2. Department of Ultrasound, Senior Department of Oncology, Chinese PLA General Hospital, Beijing 100039, China.
3. Senior Department of Cardiology, Chinese PLA General Hospital, Beijing 100039, China.
- Publication Type:Journal Article
- Keywords:
hepatitis B virus;
lipid metabolism disorders;
metabolic dysfunction-associated fatty liver disease;
metabolomics;
oral microbiota;
oral-liver axis
- MeSH:
Humans;
Lipid Metabolism;
Prospective Studies;
Microbiota;
Hepatitis B, Chronic/microbiology*;
Male;
Female;
Adult;
Fatty Liver/microbiology*;
Middle Aged;
Mouth/microbiology*;
Metabolomics
- From:
Journal of Southern Medical University
2025;45(9):2034-2045
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the impact of hepatitis B virus (HBV) infection on oral microbiota and metabolites in patients with metabolic dysfunction-associated fatty liver disease (MAFLD) and the underlying mechanisms.
METHODS:This prospective study was conducted in 47 MAFLD patients complicated with chronic hepatitis B (CHB) and 48 MAFLD patients without CHB enrolled from November, 2023 to January, 2024. Fasting tongue coating samples were collected from the patients for analyzing microbial community structures and metabolites using high-throughput 16S rDNA sequencing and non-targeted metabolomics techniques, and their associations with clinical indicators and biological pathways were explored using correlation analysis and functional annotation.
RESULTS:The levels of fasting blood glucose, total cholesterol (TC), gamma-glutamyl transferase (GGT), and severity of fatty liver were all significantly lower in MAFLD+CHB group than in MAFLD group. Microbiota analysis showed that the abundances of Patescibacteria (at the phylum level), Hydrogenophaga, and Absconditabacteriales (at the genus level) were significantly increased, while the abundance of Megasphaera was decreased in MAFLD+CHB group. The differential microbiota were significantly correlated with TC, GGT and low-density lipoprotein (r=-0.68‒0.75). Metabolomics analysis revealed that 469 metabolites (including lipids and amino acids) were upregulated and 2306 (including organic oxygen-containing compounds and phenylpropanoids) were downregulated in MAFLD+CHB group, for which KEGG enrichment analysis suggested abnormal activation of the linoleic acid metabolism and glycerophospholipid metabolism pathways. Correlation analysis between microbiota and metabolites indicated that Patescibacteria and Megasphaera, which were positively correlated with lipid metabolites and negatively with fatty acid metabolites, respectively, jointly affected glycolipid metabolism and oxidative stress pathways.
CONCLUSIONS:Compared to patients with MAFLD alone, MAFLD patients with concurrent chronic HBV infection showed lower levels in some lipid metabolism indicators and the degree of hepatic steatosis, accompanied by alterations in oral microbiota structure and metabolic profiles. The precise mechanisms involved require further investigation to be fully elucidated.
