Multi-Omics Analysis Reveals Causal Relationships and Potential Mediators Between Dietary Preferences and Risk of NAFLD

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Non-alcoholic fatty liver disease (NAFLD) is a prevalent condition closely associated with obesity and metabolic syndrome, with its global incidence on the rise. This study aims to explore the causal relationship between dietary preferences and NAFLD risk using multi-omics analysis, and to comprehensively explore possible mediating factors and their underlying mechanisms. We analyzed data from genome-wide association studies (GWAS) to assess the potential genetic links between various dietary preferences and NAFLD. A two-step Mendelian randomization (MR) analysis was conducted to evaluate whether dietary preferences affect NAFLD risk by regulating inflammatory factors. Further, co-localization analysis was used to identify gene loci driving the causal relationships between dietary preferences and NAFLD risk. Finally, clinical cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) and bioinformatics analysis were used to validate the findings.MR analysis revealed that a preference for a low-calorie diet significantly reduces NAFLD risk by modulating DNER. Co-localization analysis identified the FTO gene variant rs28429148 as a key driver of the causal relationship between soft cheese and fruit juice preferences, with soft cheese increasing and fruit juice reducing NAFLD risk. These findings were further validated by clinical cross-sectional and b

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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