Toxins to treatments: Impact of environmental pollutants, gut microbiota, and natural compounds on non-alcoholic fatty liver disease progression

Table 1 Key studies linking heavy metals, gut microbiota, and selenium in non-alcoholic fatty liver disease

Metal	Study design	Model	Key findings
Cadmium exposure and NAFLD[189]	Animal study	HFD-fed mice + Cd	Cadmium worsened hepatic lipid accumulation and gut dysbiosis; increased Proteobacteria, decreased Lactobacillus
Pb exposure and gut-liver axis[190]	Animal study	Pb-exposed mice	Pb caused intestinal barrier dysfunction, elevated LPS, aggravated hepatic inflammation and steatosis
Selenium supplementation[191]	Animal study	HFD-fed mice	Selenium improved hepatic lipid metabolism, increased Akkermansia, improved antioxidant enzyme activity
Selenium and gut microbiota[192]	Animal study	HFD-fed mice	Selenium enriched SCFA-producing microbiota; reduction in hepatic TGs, decline in inflammatory cytokines
Arsenic exposure and microbiome[193]	Animal study	Mice + arsenic	Arsenic altered microbiota composition, increased gut permeability and promoted liver fibrosis
Cadmium, microbiota, and liver injury[189,194]	Animal study	Cd-exposed mice	Cd exposure induced Firmicutes/Bacteroidetes imbalance; elevation in inflammatory cytokines and liver damage
Selenium nanoparticles in NAFLD[195]	Animal study	HFD + SeNPs	SeNPs improved oxidative stress, modulated microbiota, and reduced NAFLD severity
Selenium status and NAFLD/NASH[166]	Meta-analysis	Human studies	Low selenium significantly associated with NAFLD and NASH risk; supplementation showed mixed results

NAFLD: Non-alcoholic fatty liver disease; SCFA: Short-chain fatty acid; NASH: Non-alcoholic steatohepatitis; HFD: High-fat diet; Cd: Cadmium; Pb: Lead; LPS: Lipopolysaccharide; TG: Triglyceride; SeNP: Selenium nanoparticles.