Department of Rehabilitation, Nutrition and Sport, La Trobe University, Bundoora, Victoria, Australia.
Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia.
Nutr Rev. 2019 Nov 1;77(11):765-786. doi: 10.1093/nutrit/nuz029.
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver disorders, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), with inflammation acting as a key driver in its pathogenesis and progression. Diet has the potential to mediate the release of inflammatory markers; however, little is known about the effects of various diets.
This systematic review aimed to evaluate the effect of dietary interventions on cytokines and adipokines in patients with NAFLD.
The electronic databases MEDLINE, EMBASE, CINAHL, and Cochrane Library were searched for clinical trials investigating dietary interventions, with or without supplementation, on cytokines and adipokines in NAFLD patients.
Basic characteristics of populations, dietary intervention protocol, cytokines, and adipokines were extracted for each study. Quality of evidence was assessed using the American Dietetic Association criteria.
Nineteen studies with a total of 874 participants were included. The most frequently reported inflammatory outcomes were C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), adiponectin, and leptin. Hypocaloric, isocaloric, or low-fat diets significantly (P < 0.05) lowered levels of CRP, TNF-α, and adiponectin. The addition of nutraceutical or pharmacological supplementation to dietary interventions appeared to elicit additional benefits for all of the most frequently reported inflammatory markers.
Hypo- or isocaloric diets alone, or with co-interventions that included a nutraceutical or pharmacological supplementation, appear to improve the inflammatory profile in patients with NAFLD. Thus, anti-inflammatory diets may have the potential to improve underlying chronic inflammation that underpins the pathophysiological mechanisms of NAFLD. In the absence of any known liver-sensitive markers, the use of cytokines and adipokines as a surrogate marker of liver disease should be further investigated in well-controlled trials.
非酒精性脂肪性肝病（NAFLD）代表了一系列肝脏疾病，从单纯性脂肪变性到非酒精性脂肪性肝炎（NASH）不等，炎症是其发病机制和进展的关键驱动因素。饮食有可能调节炎症标志物的释放；然而，人们对各种饮食的影响知之甚少。
本系统评价旨在评估饮食干预对 NAFLD 患者细胞因子和脂肪因子的影响。
检索了 MEDLINE、EMBASE、CINAHL 和 Cochrane 图书馆的临床试验数据库，以调查饮食干预（有或无补充剂）对 NAFLD 患者细胞因子和脂肪因子的影响。
对每项研究的人群基本特征、饮食干预方案、细胞因子和脂肪因子进行了提取。使用美国饮食协会标准评估证据质量。
共纳入 19 项研究，总计 874 名参与者。报告最多的炎症结局是 C 反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）、白细胞介素 6（IL-6）、脂联素和瘦素。低热量、等热量或低脂肪饮食可显著（P < 0.05）降低 CRP、TNF-α 和脂联素水平。营养补充剂或药物补充剂与饮食干预联合应用似乎对所有最常报告的炎症标志物都有额外的益处。
单独进行低热量或等热量饮食，或进行包括营养补充剂或药物补充剂的联合干预，似乎可以改善 NAFLD 患者的炎症特征。因此，抗炎饮食可能有潜力改善潜在的慢性炎症，这是 NAFLD 病理生理机制的基础。在没有任何已知的肝脏敏感标志物的情况下，应进一步在对照良好的试验中研究细胞因子和脂肪因子作为肝脏疾病的替代标志物。
