Search Results (2,488)

Background and Objectives: Obstructive sleep apnea (OSA) is a clinically relevant comorbidity in both alcoholic fatty liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD). However, whether its impact differs between these etiologies remains unclear. This study directly compared OSA risk in patients with AFLD and NAFLD to elucidate its role in disease progression. Materials and Methods: We conducted a retrospective cohort study using the TriNetX research network. Adults aged ≥ 20 years with newly diagnosed AFLD or NAFLD between 2006 and 2020 were included. Propensity score matching was applied to balance demographic and clinical covariates. The primary endpoint was incident OSA, assessed at 1-, 2-, 3-, and 5-year intervals, and cumulatively through 28 September 2025. Effect estimates were expressed as relative risk, odds ratio and hazard ratio (HR). Results: Before matching, 896,302 NAFLD and 12,694 AFLD patients were identified; after 1:1 PSM, 11,583 patients remained in each group with balanced baseline characteristics. NAFLD patients consistently demonstrated higher OSA risk. Post-matching, OSA incidence became significantly elevated from year 2 onward (HR at 2 years = 1.764) and persisted at 3 years (HR = 2.078), 5 years (HR = 1.950), and cumulative follow-up (HR = 1.940). Conclusions: NAFLD confers nearly double the long-term OSA risk compared with AFLD. These findings support longitudinal OSA screening and targeted risk reduction strategies in NAFLD populations. Full article

Nonalcoholic fatty liver disease (NAFLD) associated with high-fat diet (HFD) intake involves oxidative stress, inflammation, apoptosis, and genotoxicity. Carvacrol, a natural monoterpenoid phenol, exhibits potent antioxidant, anti-inflammatory, and cytoprotective properties, but its clinical application is limited by poor solubility and bioavailability. Chitosan nanoparticles, known for their biocompatibility and ability to enhance drug delivery, offer a promising nanotherapeutic platform for carvacrol delivery in NAFLD. Given the limited therapeutic options for NAFLD, there is a growing interest in nanotherapeutic strategies to enhance the delivery and efficacy of natural antioxidants. This study examined carvacrol-loaded chitosan nanoparticles (CRV-CNPs) in HFD-induced NAFLD. Sixty rats were assigned to six groups: control, CRV-treated (100 mg/kg), CRV-CNP-treated (100 mg/kg), HFD-fed, and two combination groups receiving HFD with either CRV or CRV-CNPs (100 mg/kg) for six weeks after 14 weeks on HFD. Liver function, metabolic markers, oxidative stress parameters, antioxidant enzyme levels, inflammatory and fibrotic mediators, apoptotic gene expression, genotoxicity indices, and histopathological changes were evaluated. CRV-CNPs showed greater efficacy than free carvacrol in ameliorating hepatic dysfunction and metabolic disturbances in HFD-fed rats. CRV-CNPs significantly reduced malondialdehyde, upregulated Nrf2, and elevated hepatic glutathione peroxidase, superoxide dismutase, catalase, and reduced glutathione. Inflammatory markers (NF-κB, iNOS, IL-1β, CRP) and transforming growth factor-beta were suppressed. Pro-apoptotic genes (Bax, Caspase-3) were downregulated, while antiapoptotic Bcl-2 was upregulated. CRV-CNPs also reduced DNA fragmentation and 8-hydroxy-2′-deoxyguanosine levels, indicating strong antigenotoxic effects. Histopathological and ultrastructural assessments revealed mitigated steatosis, preserved hepatic architecture, and maintained mitochondrial integrity. In conclusion, CRV-CNPs provide potent hepatoprotection by targeting oxidative stress, inflammation, apoptosis, and genotoxicity in NAFLD, demonstrating enhanced bioavailability, solubility, and sustained release, which support their potential as an advanced nanotherapeutic strategy for NAFLD management. Full article

Introduction: Worldwide, non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder, strongly associated with increased cardiovascular morbidity and mortality. Although patients have a preserved left ventricular ejection fraction (LVEF), individuals having NAFLD may demonstrate subclinical cardiac dysfunction. Speckle tracking echocardiography (STE) enables a more sensitive evaluation, identifying even subtle alterations of myocardial strain, compared to conventional LVEF measurements. This systematic review and meta-analysis sought to examine the relationship between NAFLD and subclinical left ventricular systolic impairment, utilizing STE-derived strain parameters. Methods: A comprehensive search of the literature was undertaken using PubMed, EMBASE, and Scopus. Observational studies evaluating patients with NAFLD through STE-derived myocardial strain parameters were included. Study quality was appraised using the Newcastle-Ottawa Scale. The primary outcomes were the mean differences (MD) in global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), global area strain (GAS), and related strain rate indices between NAFLD spectrum patients and controls. Results: A total of sixteen studies, comprising 8359 participants, were included in the analysis. Compared to controls, patients with NAFLD demonstrated significant reductions in GLS (MD: −2.043; 95% CI: −2.868, −1.218), GAS (MD: −3.706; 95% CI: −4.999, −2.413), and GCS (MD: −1.415; 95% CI: −2.893, 0.064). These reductions were more substantial among individuals with moderate to severe NAFLD and those with concomitant type 2 diabetes mellitus (GLS MD: −4.385; 95% CI: −5.400, −3.369 in diabetic NAFLD vs. diabetic controls). Subgroup analysis further revealed a progressive deterioration in strain parameters from simple steatosis to more severe NAFLD. Notably, LVEF remained preserved in all groups, highlighting the subclinical nature of this dysfunction. Conclusions: This meta-analysis verifies the presence of subclinical left ventricular systolic dysfunction in individuals with NAFLD, which is identifiable by STE despite preserved LVEF. Myocardial strain metrics, particularly GLS, serve as sensitive early markers of myocardial impairment. Routine application of STE in the clinical assessment of NAFLD may support earlier cardiovascular risk detection and timely intervention. Full article

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder in Western countries, characterized by excessive fat storage in the form of lipid droplets (LDs) in hepatocytes; it is also called Metabolic-Associated Steatotic Liver Disease (MASLD), if coexisting with at least one cardiometabolic risk factor. Bergamot polyphenols (BPF) have been shown to counteract hepatic LD accumulation through potent lipogenesis suppression and associated metabolic benefits in Wistar rats, but their liver-specific anti-lipogenic effects may be species- and strain-dependent. Results and Methods: To address this issue we examined the effect of a cafeteria diet (CAF) and BPF in C3H/HeOuJ mice, which are considered resistant to diet-induced MASLD and fibrosis. Interestingly, a 15-week CAF diet led to a robust LD accumulation, weak portal and focal inflammation, and induced a higher expression of lipogenesis (Acly)- but not fibrosis-related (Col1a) genes in C3H/HeOuJ livers. This was associated with a significant increase in blood glucose, triglycerides, and total cholesterol levels, and a decrease in caecal short-chain fatty acids (SCFAs). Importantly, mice co-treated with BPF showed strongly reduced steatosis compared to CAF mice, lower blood glucose and triglyceride levels, stimulation of hepatic autophagy, and a reduced Acly gene and protein expression, followed by a more than doubled and tripled production of total SCFAs and butyric acid, respectively. Conclusions: In conclusion, while CAF diet supplementation in C3H/HeOuJ mice proves to be a suitable model of MASLD with deficient SCFA production, BPF confirms its potency to prevent murine MASLD by pleiotropic mechanisms, including beneficial effects on SCFA content, hepatic autophagy, and lipogenesis. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic hepatic disease with a rising global prevalence (25–38% of the general population). As a new term, MASLD was introduced in 2023 to replace the previous nomenclature of non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD). This new term/definition introduced changes in the diagnostic criteria and underscores the direct link between cardio-metabolic risk and this prevalent liver disease. In this context, the present review examines the clinical and pathophysiological links between MASLD and cardiovascular disease (CVD), providing a robust evidence synthesis of primarily systematic review data on the association between MASLD and coronary artery disease (CAD), atrial fibrillation (AF), and heart failure (HF). This association appears to be not only synergistic, but also independent of other known CVD risk factors, highlighting MASLD as a key cardio-metabolic risk factor that merits prompt diagnosis and treatment. The development of MASLD-related cardiovascular morbidity increases with the severity of the underlying hepatic pathology, particularly with progression to steatohepatitis and fibrosis. Notably, growing evidence highlights the links between MASLD and CVD through cardiac structural, electrical, and functional alterations that can progress to CAD, AF, and new-onset HF. Recognizing these links in clinical practice underscores the importance of early detection and multi-disciplinary management of MASLD to prevent disease progression and CVD complications. Full article

Quercetin, a dietary flavonoid, has demonstrated antioxidant, anti-inflammatory, and anti-tumor activities. Increasing evidence highlights that its metabolites contribute to these health benefits. This review summarizes current knowledge on the molecular mechanisms and therapeutic potential of quercetin and its metabolites in non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC), with a focus on redox modulation and microbiota interactions. Substantial preclinical evidence supports the protective effects of quercetin and its metabolites in NAFLD and HCC. However, clinical translation is hampered by poor bioavailability, potential redox–drug interactions, and incomplete understanding of the precise molecular mechanisms involved. Future research should prioritize further elucidating the molecular mechanisms, as they represent the foundation for the rational use of quercetin and metabolite-based derivatives in the prevention and treatment of liver-related diseases. In particular, strategies that direct the activity of these bioactive compounds to their desired sites of action—by exploiting differences between normal and cancer cells—warrant more in-depth investigation. Full article

Backgrounds: Non-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder that has become a prominent public health problem worldwide. As a traditional Chinese medicine formula, the ErChen decoction (ECD) possesses significant effects on metabolic syndrome. Methods: To determine whether ECD can relieve lipid accumulation and insulin resistance (IR) in liver cells, NAFLD and IR cell models were established by treating HepG2 cells with free fatty acids and an overdose of insulin, respectively. Bioinformatics and experimental evidence demonstrated that ECD could ameliorate NAFLD by modulating multiple pathways. The optimal combination of the key compounds in ECD was identified by the orthogonal experiment. Results: For lipid homeostasis, ECD suppressed de novo lipogenesis and reduced the cholesterol level by activating the AMPK signaling pathway. Concurrently, ECD enhanced hepatic β-oxidation by inducing PPARα-mediated upregulation of ACOX-1 and CPT-1α. ECD also resolved hepatic insulin resistance by activating the IRS1-Akt-FoxO1 pathway. The combined treatment with 100 μM liquiritin (LQ), 200 μM glycyrrhizic acid (GA) and 200 μM hesperidin (HEN) exhibited the best effect in reducing TG content in NAFLD model cells. Conclusions: ECD exhibited superior activities in activating the AMPK signaling pathway compared to the optimal compound combination. The comparison between the ECD and its key compounds demonstrated the superior synergistic effects of the herbs in ECD. Full article

Background/Objectives: Ultra-processed food (UPF) consumption is increasingly implicated in metabolic diseases; however, evidence for non-alcoholic fatty liver disease (NAFLD) and potential sex differences remains limited. Thus, this study aimed to examine the relationship between UPF consumption and NAFLD stratified by sex in Korean adults. Methods: This was a cross-sectional analysis of Korean adults from the Korea National Health and Nutrition Examination Survey 2013–2021 (n = 24,587). UPF intake was quantified as the percentage of NOVA Group 4 items consumed in total daily food weight based on a 24 h recall. The participants were grouped into quartiles of UPF intake. NAFLD was defined using the hepatic steatosis index. Survey-weighted models were used to summarize the characteristics and estimated odds ratios (ORs) for NAFLD across the UPF quartiles with adjustment for factors associated with both NAFLD and dietary intake. Linear trend tests across quartiles and continuous analyses of UPF intake were performed, with sex-stratified models to assess potential effect modification. Results: NAFLD prevalence increased as UPF intake quartile increased, from 19.1% in Q1 to 24.1% in Q4. With Q1 as reference, the fully adjusted OR for Q4 was 1.24 (95% CI, 1.10–1.41, p for trend = 0.001). In the sex-stratified analyses, the association was only significant in women (Q4 vs. Q1: OR, 1.52, 95% CI, 1.28–1.81; p for trend < 0.001). When UPF intake was modeled as a continuous variable, NAFLD risk showed a modest overall increase, with a nearly flat pattern in men and a clear linear increase in women. Conclusions: Higher UPF intake is associated with a greater risk of NAFLD in Korean adults, with a more pronounced association in women. Thus, UPF consumption is a feasible modifiable target for liver health. Full article

Background: Periodontal dysbiosis contributes to liver injury through systemic inflammation, oral–gut microbial translocation, and endotoxemia. Lipopolysaccharides (LPSs) and virulence factors derived from periodontal pathogens, particularly Porphyromonas gingivalis (P. gingivalis) activate Toll-like receptor (TLR) signaling, trigger NF-κB-mediated cytokine release (e.g., TNF-α, IL-1β, IL-6), and promote oxidative stress and Kupffer cell activation within the liver. The present systematic review summarized clinical evidence supporting these mechanistic links between periodontal pathogens and hepatic outcomes, highlighting the role of microbial crosstalk in liver pathophysiology. Methods: A PRISMA-compliant systematic review was conducted by searching PubMed, Scopus, and the Cochrane library, as well as gray literature. Eligible study designs were observational studies and trials evaluating P. gingivalis and other periodontal pathogens (Aggregatibacter actinomycetemcomitans, Prevotella intermedia, and Tannerella forsythia) for liver phenotypes (Non-Alcoholic Fatty Liver Disease [NAFLD]/Metabolic Dysfunction-Associated Steatotic Liver Disease [MASLD], fibrosis/cirrhosis, acute alcoholic hepatitis [AAH], and Hepatocellular carcinoma [HCC]). Risk of bias was assessed using the Newcastle–Ottawa Scale adapted for cross-sectional studies (NOS-CS) for observational designs and the RoB 2 scale for single randomized controlled trials (RCTs). Due to the heterogeneity of exposures/outcomes, results were summarized narratively. Results: In total, twenty studies (2012–2025; ~34,000 participants) met the inclusion criteria. Population-level evidence was conflicting (no clear association between anti-P. gingivalis serology and NAFLD), while clinical cohorts more frequently linked periodontal exposure, particularly to P. gingivalis, to more advanced liver phenotypes, including fibrosis. Microbiome studies suggested stage-related changes in oral communities rather than the effect of a single pathogen, and direct translocation into ascitic fluid was not observed in decompensated cirrhosis. Signals from interventional and behavioral research (periodontal therapy; toothbrushing frequency) indicate a potential modifiability of liver indices. The overall methodological quality was moderate with substantial heterogeneity, precluding meta-analysis. Conclusions: Current evidence supports a biologically plausible oral–liver axis in which periodontal inflammation, often involving P. gingivalis, is associated with liver damage. Causality has not yet been proven; however, periodontal evaluation and treatment may represent a low-risk option in periodontitis-associated NAFLD. Well-designed, multicenter prospective studies and randomized trials with standardized periodontal and liver measurements are needed. Full article

Non-alcoholic fatty liver disease (NAFLD) represents a prevalent chronic hepatic disorder worldwide, with its incidence continuing to rise in recent years. At the core of its pathological progression lie multiple interconnected mechanisms, including dysregulated lipid metabolism (e.g., abnormal accumulation of triglycerides in hepatocytes), impaired insulin sensitivity (which exacerbates hepatic lipid deposition), excessive production of reactive oxygen species (ROS) leading to oxidative stress, and sustained low-grade chronic inflammation that further amplifies liver tissue damage. Saponins have emerged as a crucial research direction for NAFLD intervention due to their advantage of multi-target regulation. This review synthesizes the mode of action of commonly studied saponins, including triterpenoid saponins and steroidal saponins: they regulate lipid metabolism by inhibiting fatty acid synthesis; modulate the gut microbiota; scavenge reactive oxygen species (ROS); alleviate endoplasmic reticulum stress; exert anti-inflammatory effects by inhibiting inflammasomes; and simultaneously regulate autophagy, restrain the activation of hepatic stellate cells, and modulate the gut microbiota, thereby achieving anti-apoptotic and anti-hepatic fibrosis effects. In conclusion, saponins can synergistically intervene in NAFLD through multiple mechanisms with good safety, while low bioavailability constitutes the main bottleneck for their clinical translation. In the future, it is necessary to further optimize formulation processes to improve absorption efficiency and conduct high-quality clinical studies to verify their long-term efficacy and drug–drug interactions, thus providing a new possible direction for NAFLD treatment. Full article

The oral cavity contains a diverse group of bacteria in the saliva, as well as structured aggregates of bacterial cells on the mucosal surfaces. Oral microbiota (OM) dysbiosis not only induces local inflammation, it can also trigger systemic inflammation leading to metabolic diseases and neuropsychiatric diseases (NPDs). While primary evidence indicates that oral microbiota dysbiosis induces gut microbiota aberrations, which exacerbate inflammation associated with metabolic diseases (obesity, dyslipidemia, diabetes, nonalcoholic fatty liver disease (NAFLD), and insulin resistance), other studies revealed the contribution of the oral microbiota–brain axis in the pathogenesis of NPDs. GM dysbiosis and inflammation also induce epigenetic alterations in cytokine genes, such as IL-1β, IL-6, TNF-α, NF-kB, BTLA, IL-18R1, TGF-β, P13k/Akt1, Ctnnb1, and Hsp90aa1, as well as DNMTs, HDACs, and DAT1 associated with the development and progression of metabolic disorders and/or NPDs. Therefore, the epigenome could serve as a target for preventive or therapeutic interventions. Here, we (i) review emerging evidence of the potential impact of OM dysbiosis in the pathogenesis of metabolic diseases and NPDs, (ii) highlight the relationship between OM-induced inflammation and epigenetic alterations driving NPDs pathogenesis and interlinked metabolic aberrations, (iii) discuss therapeutic approaches capable of treating metabolic diseases and NPDs through reshaping the microbiota and its epigenetic metabolites, and hence mitigating epigenetic aberrations linked to metabolic diseases and NPDs. Finally, we outline challenges and current research gaps related to investigating the relationship between microbiota, epigenetic aberrations, and metabolic abnormalities associated with NPDs. Full article

Nowadays, nonalcoholic fatty liver disease (NAFLD) represents the most common cause of chronic liver disorder worldwide. From the clinical point of view, it evolves from steatosis to nonalcoholic steatohepatitis, which can lead to cirrhosis and finally to hepatocellular carcinoma. The mechanisms involved in its progression to more pathological stages and NAFLD pathogenesis are not completely understood. The research concerning NAFLD has become urgent and important because the age of NAFLD diagnosis is progressively decreasing, and its relationship with cancer risk is already well known. Because NAFLD ultimately leads to disability and imposes a major socioeconomic burden, timely diagnosis and effective treatment of NAFLD is particularly important. In the development of NAFLD, noncoding RNAs (ncRNAs) represented by microRNAs, long noncoding RNAs, circular RNAs, and piRNAs are epigenetic factors that play important regulatory roles. In the current review, we present updated information regarding the role of miRNAs, lncRNAs, circRNAs, and piRNAs, aiming to develop a good understanding of their regulatory functions in hepatic metabolism and concerning their potential use as biomarkers for early NAFLD/NASH diagnosis and as therapeutic targets. Full article

Aim: This current research aims to determine the predictive value of the ratio of triglyceride (TG)/high-density lipoprotein cholesterol (HDL-C), index of triglyceride–glucose (TyG), homeostatic model assessment for insulin resistance (HOMA-IR) score, and anthropometric measurements at the onset of non-alcoholic fatty liver disease (NAFLD) in obese kids and juveniles. It also sought to assess how novel cardiovascular risk markers are affected in obese pediatric patients with NAFLD. Materials and Methods: Between November 2024 and May 2025, a total of 199 pediatric patients were prospectively evaluated, including 150 children with obesity and 49 entirely healthy controls. Two categories of obese patients were created based on whether or not they had non-alcoholic fatty liver disease. These groups were compared with each other and with the control group in terms of HOMA-IR score, index of TyG, ratio of TG/HDL-C, anthropometric parameters (percentage of body fat [BFP], index of body mass [BMI], body fat mass [BFM], waist circumference [WC]), and cardiovascular risk markers. The cutoff values, sensitivity, and specificity of the HOMA-IR score, ratio of TG/HDL-C, anthropometric measurements, and index of TyG in predicting NAFLD were assessed using Receiver Operating Characteristic (ROC) analysis. Results: Obese kids and juveniles with NAFLD had significantly higher TG/HDL-C ratios, TyG indices, HOMA-IR scores, anthropometric measurements, and cardiovascular risk markers than those without NAFLD (p < 0.001). The TG/HDL-C ratio (AUC: 0.936; 81.8% sensitivity, 95.9% specificity) and the TyG index (AUC: 0.912; 81.8% sensitivity, 91.8% specificity) showed strong predictive value for NAFLD, while HOMA-IR and WC were found to be relatively weaker predictors. Conclusions: The index of TyG and ratio of TG/HDL-C are highly effective parameters in predicting NAFLD development in obese kids and juveniles. Those with increased WC and BFP should be closely monitored for NAFLD development. Pediatric patients with NAFLD should be carefully followed up for potential cardiovascular diseases. Full article

Background/Objectives: Lifestyle-related diseases such as obesity, diabetes, hypertension, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), and osteoarthritis disproportionately affect women due to hormonal, metabolic, and socio-cultural factors. Emerging evidence suggests that combining structured exercise with nano-curcumin, a bioavailable phytochemical formulation with potent antioxidant and anti-inflammatory properties, may provide synergistic benefits. This scoping review systematically synthesizes available evidence on the combined effects of nano-curcumin supplementation and exercise interventions on health outcomes in women with lifestyle-related diseases. Methods: Following the Joanna Briggs Institute methodology and the PRISMA-ScR framework, a comprehensive database search was conducted in March 2025 and updated in June 2025. Records were retrieved from Scopus (n = 30), Web of Science (n = 22), PubMed (n = 18), and other sources (n = 71), yielding a total of 141 studies. After screening and deduplication, eight studies met the inclusion criteria and were included in this review. All the studies were conducted in Iran with small sample sizes (12–53 participants) and short intervention durations (6–16 weeks). Therefore, the current evidence is geographically and demographically limited. Results: Across the included trials, the combined interventions produced additive or synergistic improvements in oxidative stress markers, inflammatory cytokines, lipid and glucose metabolism, cardiovascular function, pulmonary capacity, muscle fitness, and psychological outcomes (e.g., depression). When paired with nano-curcumin supplementation at different concentrations, high-intensity interval training, aerobic exercise, Pilates, and resistance training consistently outperformed exercise or supplementation alone in modulating antioxidant defenses, reducing systemic inflammation, and improving metabolic risk factors. Conclusions: The integration of exercise and nano-curcumin supplementation appears to confer superior benefits for women with lifestyle-related diseases compared with either approach alone. These findings highlight the potential of combining phytochemicals with lifestyle interventions to optimize women’s health outcomes. However, most available evidence originates from small, short-term studies in single geographic regions. Large-scale, multicenter, randomized controlled trials with diverse populations are warranted to establish standardized protocols and optimal dosing strategies, and to assess long-term safety and efficacy. Full article

Background: Strobilurin fungicides (SFs) are widely detected in the environment, but data on their occurrence in humans and potential health effects are scarce. Objective: This study aimed to characterize the exposure to SFs in a human population from South China and to investigate their potential association with biomarkers of oxidative stress and liver damage. Methods: In a cross-sectional study, we analyzed serum samples from healthy participants and secondary nonalcoholic fatty liver disease (S-NAFLD) patients. Concentrations of SFs and oxidative stress biomarkers including 8-iso-prostaglandin-F2α (8-PGF_2α), 11β-prostaglandin F2α (11-PGF_2α), 15(R)-prostaglandin F2α (15-PGF_2α), and 8-oxo-7,8-dihydro-20-deoxyguanosine (8-OHdG) were measured. Associations between SF exposure, liver function biomarkers, and S-NAFLD prevalence were assessed using multivariate regression models. A mediation analysis was conducted to explore the role of oxidative stress. Results: Azoxystrobin (AZ), fluoxastrobin (FLUO), and fenamidone (FE) were the predominant compounds, with median concentrations ranging from 0.016 to 0.042 ng/mL. Significant positive correlations were observed between all frequently detected SFs and oxidative stress biomarkers (p < 0.05). FE was associated with a modest, albeit statistically significant, prevalence of S-NAFLD. AZ and FE were also found to be statistically significantly associated with altered levels of direct bilirubin (DBIL, FDR-q < 0.05). The exploratory mediation analysis indicated a statistically significant indirect effect (17.1% to 31.2%), suggesting that lipid peroxidation biomarkers could serve as potential mediators between AZ exposure and DBIL levels. Conclusions: This study provides the first evidence of widespread SF exposure in a South Chinese population and reveals significant associations with oxidative stress and AZ exposure with liver function biomarkers (i.e., DBIL), with exploratory analyses suggesting a potential mediating role of oxidative stress in this relationship. However, the cross-sectional design precludes causal inference, and the modest effect sizes warrant cautious interpretation. These findings highlight the need for further longitudinal research to confirm the hepatotoxicity of SFs in humans. Full article