Feldman Alexandra, Aigner Elmar, Weghuber Daniel, Paulmichl Katharina
First Department of Medicine, Paracelsus Medical University, Müllner Hauptstrasse 48, 5020 Salzburg, Austria ; Obesity Research Unit, Paracelsus Medical University, Müllner Hauptstrasse 48, 5020 Salzburg, Austria.
Obesity Research Unit, Paracelsus Medical University, Müllner Hauptstrasse 48, 5020 Salzburg, Austria ; Department of Pediatrics, Paracelsus Medical University, Müllner Hauptstrasse 48, 5020 Salzburg, Austria.
Biomed Res Int. 2015;2015:287401. doi: 10.1155/2015/287401. Epub 2015 Jul 26.
Obesity is a rapidly growing health problem and is paralleled by a multitude of comorbidities, including nonalcoholic fatty liver disease (NAFLD). NAFLD has become the most common chronic liver disease in both adults and children. The current understanding of NAFLD is still fragmentary. While simple steatosis is characterized by the interplay between excessive free fatty acid accumulation and hepatic insulin resistance, the progression to NASH has been related to oxidative stress and a proinflammatory state with dysbalanced adipokine, cytokine levels, and endotoxin-mediated immune response. In addition, oxidative stress has been suggested to play a central role for the sequelae leading to NASH. Trace elements are critical in regulatory, immunologic, and antioxidant functions resulting in protection against inflammation and peroxidation and consequently against the known comorbidities of obesity. Disruptions of the metal detoxification processes located in the liver are plausibly related to NAFLD development via oxidative stress. Perturbations of iron and copper (Cu) homeostasis have been shown to contribute to the pathogenesis of NAFLD. This review presents current data from pediatric studies. In addition, data from adult studies are summarized where clinical relevance may be extrapolated to pediatric obesity and NAFLD.
肥胖是一个迅速发展的健康问题,同时伴有多种合并症,包括非酒精性脂肪性肝病(NAFLD)。NAFLD已成为成人和儿童中最常见的慢性肝病。目前对NAFLD的认识仍然支离破碎。虽然单纯性脂肪肝的特征是过量游离脂肪酸积累与肝脏胰岛素抵抗之间的相互作用,但向非酒精性脂肪性肝炎(NASH)的进展与氧化应激、脂肪因子、细胞因子水平失衡以及内毒素介导的免疫反应所导致的促炎状态有关。此外,氧化应激被认为在导致NASH的后遗症中起核心作用。微量元素在调节、免疫和抗氧化功能中至关重要,可防止炎症和过氧化,从而预防肥胖的已知合并症。肝脏中金属解毒过程的破坏可能通过氧化应激与NAFLD的发展有关。铁和铜(Cu)稳态的紊乱已被证明有助于NAFLD的发病机制。本综述展示了儿科研究的当前数据。此外,还总结了成人研究的数据,这些数据的临床相关性可外推至儿童肥胖和NAFLD。