Sedighi Mohammad, Saber Amir, Bagheri Amir, Hazratian Saba, Pasdar Yahya, Najafi Farid, Moradinazar Mehdi, Soleimani Davood
Nutritional Sciences Department, School of Nutrition Sciences and Food Technology, Kermanshah University of Medical Sciences, Dolat-Abad Street, Isar Square, Kermanshah, Iran.
Research Center for Environmental Determinants of Health, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Nutr Metab (Lond). 2025 Jan 20;22(1):5. doi: 10.1186/s12986-025-00897-1.
Persistent inflammation plays a crucial role in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to scrutinize the associations of diet-induced inflammation with the improvement or worsening of hepatic steatosis and fibrosis in MASLD.
This longitudinal study involved 2,537 participants from the Ravanser Non-Communicable Disease (RaNCD) cohort (2015-2023). Dietary intake was assessed using the 118-item food frequency questionnaire (FFQ), and diet-induced inflammation was determined using the dietary inflammatory index (DII). The AST to platelet ratio index (APRI) and Fibrosis-4 (FIB-4) were used as confirmed predictive indicators for hepatic fibrosis and the hepatic steatosis index (HSI) was used for hepatic steatosis.
Adherence to an inflammatory diet independently increases the risk of worsening hepatic steatosis (RR:1.39; 95%CI: 1.02-1.93; P-value: 0.04) and reduces the risk of improving hepatic steatosis (RR: 66; 95% CI: 0.48-0.98; P-value: 0.01) compared to an anti-inflammatory diet. The DII scores did not show any connection to hepatic fibrosis, as determined by FIB-4 (β: - 1.08; 95%CI: - 2.43 to 0.27; P-value: 0.12) and APRI (β: 0.22; 95%CI: - 1.51 to 1.95; P-value: 0.80).
These results underscore the importance of dietary composition in managing hepatic steatosis and highlight the need for further research to explore the mechanisms underlying these associations.
持续性炎症在代谢功能障碍相关脂肪性肝病（MASLD）的发病机制中起关键作用。我们旨在研究饮食诱导的炎症与MASLD患者肝脂肪变性和纤维化改善或恶化之间的关联。
这项纵向研究纳入了来自拉万塞尔非传染性疾病（RaNCD）队列（2015 - 2023年）的2537名参与者。使用118项食物频率问卷（FFQ）评估饮食摄入量，并使用饮食炎症指数（DII）确定饮食诱导的炎症。谷草转氨酶与血小板比值指数（APRI）和纤维化-4（FIB-4）用作肝纤维化的确诊预测指标，肝脂肪变性指数（HSI）用于评估肝脂肪变性。
与抗炎饮食相比，坚持炎症性饮食会独立增加肝脂肪变性恶化的风险（RR：1.39；95%CI：1.02 - 1.93；P值：0.04），并降低肝脂肪变性改善的风险（RR：0.66；95%CI：0.48 - 0.98；P值：0.01）。DII评分与通过FIB-4（β： - 1.08；95%CI： - 2.43至0.27；P值：0.12）和APRI（β：0.22；95%CI： - 1.51至1.95；P值：0.80）确定的肝纤维化无任何关联。
这些结果强调了饮食组成在管理肝脂肪变性中的重要性，并突出了进一步研究以探索这些关联背后机制的必要性。
