Frontiers in microbiology · 2026
Combined exposure to silica nanoparticles and high-fat diet modulates metabolism-associated fatty liver disease via the gut-liver axis.
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Zhang XueYan, Chen Kaifeng, Liang Yifan, Sun Shuo, Chen Junjie, Wang Qian, Wang Fenghong, Zhang Lei
Аннотация
BACKGROUND: The increasing prevalence of metabolism-associated fatty liver disease (MAFLD) is associated with environmental pollutants and dietary factors, yet the synergistic effect and underlying mechanism of silica nanoparticles (SiNP) and a high-fat diet (HFD) remain unclear.
METHODS: This study aimed to investigate the role of the gut-liver axis in MAFLD pathogenesis induced by co-exposure to SiNP and HFD, utilizing a multi-omics approach.
RESULTS: In this study, we found that combined SiNP and HFD exposure exacerbated liver injury, as evidenced by significant steatosis, inflammatory infiltration, fibrosis, and elevated serum ALT/AST levels. It impaired intestinal barrier integrity and induced gut microbiota dysbiosis, characterized by altered microbial richness and differential abundance of specific bacteria. Liver metabolomics revealed significant perturbations, with the riboflavin metabolism pathway being the most notably enriched. Key metabolites in this pathway, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) showed dose-dependent alterations. Correlation analysis underscored a strong link between specific gut microbes and riboflavin metabolism intermediates. Network toxicology identified six hub targets-IL-6, IL-1β, Casp3, Pparγ, Alb, and Tgfβ1 within the riboflavin metabolism network, and molecular docking confirmed their strong binding affinities with FMN and FAD.
CONCLUSION: These findings demonstrated that combined exposure to SiNP and HFD induced gut-liver axis dysfunction and exacerbated MAFLD progression, which was mainly attributed to gut microbiota dysbiosis-mediated disruption of riboflavin metabolism. Our study highlighted the gut microbiota-riboflavin axis as a potentially promising intervention strategy for MAFLD, and identifies possible targets for the prevention and treatment of MAFLD.
METHODS: This study aimed to investigate the role of the gut-liver axis in MAFLD pathogenesis induced by co-exposure to SiNP and HFD, utilizing a multi-omics approach.
RESULTS: In this study, we found that combined SiNP and HFD exposure exacerbated liver injury, as evidenced by significant steatosis, inflammatory infiltration, fibrosis, and elevated serum ALT/AST levels. It impaired intestinal barrier integrity and induced gut microbiota dysbiosis, characterized by altered microbial richness and differential abundance of specific bacteria. Liver metabolomics revealed significant perturbations, with the riboflavin metabolism pathway being the most notably enriched. Key metabolites in this pathway, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) showed dose-dependent alterations. Correlation analysis underscored a strong link between specific gut microbes and riboflavin metabolism intermediates. Network toxicology identified six hub targets-IL-6, IL-1β, Casp3, Pparγ, Alb, and Tgfβ1 within the riboflavin metabolism network, and molecular docking confirmed their strong binding affinities with FMN and FAD.
CONCLUSION: These findings demonstrated that combined exposure to SiNP and HFD induced gut-liver axis dysfunction and exacerbated MAFLD progression, which was mainly attributed to gut microbiota dysbiosis-mediated disruption of riboflavin metabolism. Our study highlighted the gut microbiota-riboflavin axis as a potentially promising intervention strategy for MAFLD, and identifies possible targets for the prevention and treatment of MAFLD.