Delgado Jorge-Shmuel
The University of Chicago, Section of Gastroenterology, Department of Medicine, Chicago, 5841 S. Maryland Ave., MC 4076 Chicago, IL 60637, USA.
Eur J Intern Med. 2008 Mar;19(2):75-82. doi: 10.1016/j.ejim.2007.02.034.
Nonalcoholic fatty liver disease (NAFLD) is one of the most common etiologies of chronic liver disease worldwide. NALFD encompasses a continuum of histological findings ranging from steatosis alone, to nonalcoholic steatohepatitis (NASH) with steatosis, inflammation, hepatocyte ballooning, fibrosis and eventually liver cirrhosis. The pathogenesis of NAFLD might be related to a deregulated cross-talk between liver and visceral adipose tissue, originating an impairment of normal insulin signaling. A better comprehension of the immunologic and metabolic roles of adipose tissue in modulating inflammatory pathways will enhance our understanding of the molecular mechanisms leading to progression of fatty liver disease. These insights, moreover, will suggest new strategies to improve insulin sensitivity and reduce obesity-associated morbidities and mortality.
非酒精性脂肪性肝病(NAFLD)是全球慢性肝病最常见的病因之一。NAFLD涵盖了一系列组织学表现,从单纯的脂肪变性到伴有脂肪变性、炎症、肝细胞气球样变、纤维化并最终发展为肝硬化的非酒精性脂肪性肝炎(NASH)。NAFLD的发病机制可能与肝脏和内脏脂肪组织之间失调的相互作用有关,从而导致正常胰岛素信号传导受损。更好地理解脂肪组织在调节炎症途径中的免疫和代谢作用,将增进我们对导致脂肪性肝病进展的分子机制的理解。此外,这些见解将为改善胰岛素敏感性以及降低肥胖相关的发病率和死亡率提供新的策略。