Tsochatzis Emmanuel A, Papatheodoridis George V, Archimandritis Athanasios J
2nd Department of Internal Medicine, Medical School of Athens University, Hippokration General Hospital, Athens, Greece.
Mediators Inflamm. 2009;2009:831670. doi: 10.1155/2009/831670. Epub 2009 Jun 3.
Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and can vary from benign steatosis to end-stage liver disease. The pathogenesis of non-alcoholic steatohepatitis (NASH) is currently thought to involve a multiple-hit process with the first hit being the accumulation of liver fat which is followed by the development of necroinflammation and fibrosis. There is mounting evidence that cytokines secreted from adipose tissue, namely, adipokines, are implicated in the pathogenesis and progression of NAFLD. In the current review, we explore the role of these adipokines, particularly leptin, adiponectin, resistin, tumor necrosis factor-a, and interleukin-6 in NASH, as elucidated in experimental models and clinical practice. We also comment on their potential use as noninvasive markers for differentiating simple fatty liver from NASH as well as on their potential future therapeutic role in patients with NASH.
非酒精性脂肪性肝病（NAFLD）是代谢综合征的肝脏表现，其范围可从良性脂肪变性到终末期肝病。目前认为，非酒精性脂肪性肝炎（NASH）的发病机制涉及多步骤过程，第一步是肝脏脂肪堆积，随后发展为坏死性炎症和纤维化。越来越多的证据表明，脂肪组织分泌的细胞因子，即脂肪因子，与NAFLD的发病机制和进展有关。在本综述中，我们探讨了这些脂肪因子，特别是瘦素、脂联素、抵抗素、肿瘤坏死因子-α和白细胞介素-6在NASH中的作用，这些作用在实验模型和临床实践中均有阐述。我们还评论了它们作为区分单纯性脂肪肝和NASH的非侵入性标志物的潜在用途，以及它们未来在NASH患者中的潜在治疗作用。
