Non-alcoholic fatty liver disease (NAFLD) is a growing public health concern associated with obesity, diabetes, and metabolic syndromes. However, awareness and preventive behaviors remain understudied among young adults in low- and middle-income countries. This cross-sectional study assesses knowledge, attitudes, and practices related to NAFLD. This study is carried out among 343 university students (predominantly undergraduate students, mean age 24.6 years) at the Islamic University of Technology(IUT), Bangladesh. Even with 76.1% awareness, knowledge was very poor (39.1%) or moderate (40.2%). This shows significant gaps in understanding risk factors, treatment, prevention, and a strong dependence on informal information sources. Knowledge was particularly associated with age, region, and educational level. Preventive measures were extremely low, with only 11.1% followed by dieting restrictions and 31.2% making lifestyle changes. In an exploratory analysis limited to the 59 students who self-reported a prior NAFLD diagnosis (a figure likely inflated by over-reporting and not clinically confirmed), nearly half (47.5%) showed poor management practices. These findings reveal significant gaps in NAFLD literacy and health behaviors among university students in Bangladesh. This underscores the urgent need for institution-based and evidence-based educational programs and awareness campaigns to promote early prevention and effective self management of NAFLD.

The LKB1-AMPK signaling pathway is a central regulator of hepatic energy homeostasis and is increasingly implicated in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). LKB1-mediated AMPK activation promotes fatty acid β-oxidation, autophagy, and mitochondrial biogenesis. At the same time, it suppresses de novo lipogenesis, cholesterol synthesis, and mTOR-dependent anabolic growth, thereby supporting hepatic lipid and energy balance. Impairment of this pathway may disrupt hepatic lipid homeostasis and promote triglyceride accumulation. Oxidative stress, microRNA dysregulation, hormonal imbalance, copper dysregulation, and inflammatory mediators can further contribute to mitochondrial injury, hepatocellular apoptosis, and inflammatory activation. These processes may facilitate progression from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, and hepatocarcinogenesis. LKB1-AMPK signaling also intersects with immunometabolic and stromal pathways. Defects in hepatic immune and stromal compartments may enhance pro-inflammatory Th17 responses and fibrogenic transformation. Therapeutically, pharmacologic activation of LKB1-AMPK has shown context-dependent cytoprotective potential, mainly in preclinical models. Natural compounds, synthetic small molecules, repurposed agents, and nutrient-derived modulators can activate LKB1-AMPK signaling. These interventions reduce steatosis, oxidative stress, and endoplasmic reticulum stress while enhancing autophagic flux and fatty acid catabolism. Additional benefits may arise through gut microbiota-mediated signaling that converges on LKB1-AMPK-dependent metabolic restoration. Overall, the LKB1-AMPK axis links nutrient sensing, mitochondrial function, redox control, and inflammatory regulation in NAFLD pathophysiology. Current evidence supports further development of pathway-targeted interventions, but clinical translation requires stronger human validation.

Objective: To explore the association between metabolic dysfunction-associated fatty liver disease (MAFLD) and myocardial ischemia in non-obese patients with suspected coronary heart disease (CAD), and to analyze the differences in this association across subgroups stratified by body mass index (BMI) and coronary artery lesion severity. Methods: This retrospective study enrolled non-obese patients (18.5 kg/m[2]≤BMI<28.0 kg/m[2]) with suspected CAD who underwent stress/rest radionuclide myocardial perfusion imaging (MPI) at the Department of Nuclear Medicine, the Third Affiliated Hospital of Soochow University between January 1, 2022 and December 31, 2024. Patients were divided into myocardial ischemia group and non-ischemia group based on MPI findings. MAFLD diagnosis was determined based on hepatic steatosis detected by low-dose CT integrated with single-photon emission computed tomography/CT (SPECT/CT), combined with established diagnostic criteria (no excessive alcohol consumption plus presence of metabolic dysfunction). Univariate and multivariate logistic regression models were applied to analyze the correlation between MAFLD and myocardial ischemia. Stratified analyses were further performed according to BMI (normal weight: 18.5 kg/m[2]≤BMI<24.0 kg/m[2]; overweight: 24.0 kg/m[2]≤BMI<28.0 kg/m[2]) and coronary angiography results (obstructive or non-obstructive CAD) to assess the relationship between MAFLD and myocardial ischemia in each subgroup. Results: A total of 271 patients with suspected CAD were enrolled, aged (61.6±10.2) years, with 143 (52.8%) males. There were 135 patients in the myocardial ischemia group and 136 in the non-ischemia group. MAFLD was diagnosed in 88 patients (32.5%). The proportion of patients diagnosed with MAFLD was higher in the myocardial ischemia group than in the non-myocardial ischemia group (61 cases (45.2%) vs. 27 cases (19.9%), P<0.001). Multivariate logistic regression analysis showed that MAFLD was independently associated with myocardial ischemia (OR=3.43, 95%CI 1.85-6.28, P<0.001). Subgroup analysis revealed that MAFLD was associated with myocardial ischemia in both normal weight group (OR=7.62, 95%CI 2.48-23.44, P<0.001) and overweight group (OR=2.60, 95%CI 1.20-5.60, P=0.015), with a stronger association observed in normal-weight individuals. This association also existed in non-obstructive CAD group (OR=6.50, 95%CI 2.23-18.94, P<0.001) and obstructive CAD group (OR=3.05, 95%CI 1.37-6.80, P=0.006). Conclusion: MAFLD acts as an independent risk factor for myocardial ischemia in non-obese patients with suspected CAD, and this association persists across subgroups stratified by BMI (normal weight vs. overweight) and coronary lesion phenotype (obstructive vs. non-obstructive CAD).

Ferulic acid (FA) is a phenolic acid found in plants, such as wheat, corn, beet, etc. It is an important active ingredient in many herbal medicines. FA has been reported to have a variety of biological activities, especially in the resistance to oxidative stress, inflammation, vascular endothelial damage, fibrosis, apoptosis, and platelet aggregation. Because FA has advantages of high activities, low cost, non-toxic, good safety and stable structure. So it is widely used in food additives, medicine, healthcare products, and cosmetics. Numerous studies have shown the protective effects of FA and its derivatives on the liver. This paper reviews the recent research progress of FA and its derivatives in preventing and curing liver damages induced by various different factors, including the effects of FA and its derivatives on physicochemical factors induced liver injury, liver tumors, alcoholic liver disease, non-alcoholic fatty liver disease, liver metabolic disorder of diabetics, and hepatotoxicity of aflatoxin B1. The aim of this review is to provide reference for the research and application of FA and its derivatives in the prevention and treatment of liver diseases.