Nelson James E, Klintworth Heather, Kowdley Kris V
Benaroya Research Institute at Virginia Mason Medical Center, Seattle, USA.
Curr Gastroenterol Rep. 2012 Feb;14(1):8-16. doi: 10.1007/s11894-011-0234-4.
Non-Alcoholic Fatty Liver Disease (NAFLD) is a common worldwide clinical and major public health problem affecting both adults and children in developed nations. Increased hepatic iron stores are observed in about one-third of adult NAFLD patients. Iron deposition may occur in parenchymal and/or non-parenchymal cells of the reticuloendothelial system (RES). Similar patterns of iron deposition have been associated with increased severity of other chronic liver diseases including HCV infection and dysmetabolic iron overload, suggesting there may be a common mechanism for hepatic iron deposition in these diseases. In NAFLD, iron may potentiate the onset and progression of disease by increasing oxidative stress and altering insulin signaling and lipid metabolism. The impact of iron in these processes may depend upon the sub-cellular location of iron deposition in hepatocytes or RES cells. Iron depletion therapy has shown efficacy at reducing serum aminotransferase levels and improving insulin sensitivity in subjects with NAFLD.
非酒精性脂肪性肝病（NAFLD）是一个全球普遍存在的临床问题，也是发达国家影响成人和儿童的主要公共卫生问题。在大约三分之一的成年NAFLD患者中观察到肝脏铁储存增加。铁沉积可能发生在网状内皮系统（RES）的实质细胞和/或非实质细胞中。类似的铁沉积模式与包括丙型肝炎病毒（HCV）感染和代谢异常性铁过载在内的其他慢性肝病的严重程度增加有关，这表明这些疾病中肝脏铁沉积可能存在共同机制。在NAFLD中，铁可能通过增加氧化应激以及改变胰岛素信号传导和脂质代谢来促进疾病的发生和发展。铁在这些过程中的影响可能取决于铁在肝细胞或RES细胞中的亚细胞定位。铁耗竭疗法已显示出在降低NAFLD患者血清转氨酶水平和改善胰岛素敏感性方面的疗效。
