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Dietary Inflammatory Potential and Metabolic (Dysfunction)-Associated Steatotic Liver Disease and Its Complications: A Comprehensive Review Publisher Pubmed



Sepehrinia M1, 2 ; Khanmohammadi S3, 5 ; Rezaei N6 ; Kuchay MS7
Authors

Source: Clinical Nutrition ESPEN Published:2025


Abstract

Metabolic (dysfunction)-associated steatotic liver disease (MASLD) represents a spectrum of liver pathologies linked to metabolic syndrome components. Inflammation emerges as a pivotal player in MASLD pathogenesis, initiating and perpetuating hepatic injury. Diet, a modifiable risk factor, influences inflammation levels and MASLD progression. This review synthesizes existing evidence on the association between pro-inflammatory diets, assessed via the Dietary Inflammatory Index (DII) and Empirical Dietary Inflammatory Potential (EDIP), and MASLD. Evidence suggests a significant association between higher DII/EDIP scores and MASLD risk, with studies revealing a positive correlation between inflammatory diet intake and MASLD occurrence, particularly in males. However, inconsistencies exist regarding the influence of body mass index (BMI) on this association and criticisms regarding adjustment for BMI and reliance on surrogate markers necessitate cautious interpretation. Limited data suggest a potential link between dietary inflammatory potential and advanced liver fibrosis and heightened risk of hepatocellular carcinoma (HCC) with increased DII/EDIP scores, albeit requiring further confirmation through gold-standard assessment methods. Dietary-induced inflammation exacerbates MASLD pathogenesis through multiple pathways, including insulin resistance, adipose tissue dysfunction, gut microbiota alterations, and oxidative stress, culminating in hepatic steatosis, inflammation, and fibrosis. Further research utilizing robust methodologies is imperative to confirm these findings and elucidate underlying mechanisms, thus informing targeted dietary interventions for MASLD management. © 2024 European Society for Clinical Nutrition and Metabolism
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