Malaguarnera Mariano, Di Rosa Michelino, Nicoletti Ferdinando, Malaguarnera Lucia
Department of Internal Medicine, University of Catania, Catania, Italy.
J Mol Med (Berl). 2009 Jul;87(7):679-95. doi: 10.1007/s00109-009-0464-1. Epub 2009 Apr 8.
Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic-related disorder characterized by fatty infiltration of the liver in the absence of alcohol consumption. NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which might progress to end-stage liver disease. This progression is related to the insulin resistance, which is strongly linked to the metabolic syndrome consisting of central obesity, diabetes mellitus, and hypertension. Earlier, the increased concentration of intracellular fatty acids within hepatocytes leads to steatosis. Subsequently, multifactorial complex interactions between nutritional factors, lifestyle, and genetic determinants promote necrosis, inflammation, fibrosis, and hepatocellular damage. Up to now, many studies have revealed the mechanism associated with insulin resistance, whereas the mechanisms related to the molecular components have been incompletely characterized. This review aims to assess the potential molecular mediators initiating and supporting the progression of NASH to establish precocious diagnosis and to plan more specific treatment for this disease.
非酒精性脂肪性肝病(NAFLD)是一种新出现的与代谢相关的疾病,其特征是在无酒精摄入的情况下肝脏出现脂肪浸润。NAFLD范围从单纯性脂肪变性到非酒精性脂肪性肝炎(NASH),后者可能进展为终末期肝病。这种进展与胰岛素抵抗有关,而胰岛素抵抗与由中心性肥胖、糖尿病和高血压组成的代谢综合征密切相关。早期,肝细胞内细胞内脂肪酸浓度增加导致脂肪变性。随后,营养因素、生活方式和遗传决定因素之间的多因素复杂相互作用促进坏死、炎症、纤维化和肝细胞损伤。到目前为止,许多研究已经揭示了与胰岛素抵抗相关的机制,而与分子成分相关的机制尚未完全明确。本综述旨在评估启动和支持NASH进展的潜在分子介质,以建立早熟诊断并为该疾病规划更具体的治疗方法。