Sepehrinia Matin, Khanmohammadi Shaghayegh, Rezaei Nima, Kuchay Mohammad Shafi
Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute (WHO Collaborating Center), Shahid Beheshti University of Medical Sciences, Tehran, Iran; Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran.
Non-Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran, Iran; University of Medical Sciences, Tehran, Iran; School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Clin Nutr ESPEN. 2025 Feb;65:162-171. doi: 10.1016/j.clnesp.2024.11.032. Epub 2024 Nov 26.
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.
代谢(功能障碍)相关脂肪性肝病(MASLD)代表了一系列与代谢综合征成分相关的肝脏病变。炎症在MASLD发病机制中起着关键作用,引发并持续肝脏损伤。饮食作为一个可改变的风险因素,会影响炎症水平和MASLD的进展。本综述综合了通过饮食炎症指数(DII)和经验性饮食炎症潜能(EDIP)评估的促炎饮食与MASLD之间关联的现有证据。证据表明,较高的DII/EDIP评分与MASLD风险之间存在显著关联,研究显示炎症性饮食摄入与MASLD发生呈正相关,尤其是在男性中。然而,关于体重指数(BMI)对这种关联的影响存在不一致之处,并且对BMI调整和依赖替代标志物的批评使得需要谨慎解读。有限的数据表明,饮食炎症潜能与晚期肝纤维化以及随着DII/EDIP评分增加肝细胞癌(HCC)风险升高之间可能存在联系,尽管需要通过金标准评估方法进一步证实。饮食诱导的炎症通过多种途径加剧MASLD发病机制,包括胰岛素抵抗、脂肪组织功能障碍、肠道微生物群改变和氧化应激,最终导致肝脏脂肪变性、炎症和纤维化。利用可靠方法进行进一步研究对于证实这些发现并阐明潜在机制至关重要,从而为MASLD管理提供有针对性的饮食干预措施。