비알코올성 지방간질환의 병인 = PG 1 : Epidemiology & pathogenesis ; Pathogenesis of Nonalcoholic Fatty Liver Disease

다국어 초록 (Multilingual Abstract)

Insulin resistance is the main pathophysiologic hall mark of Nonalcohlic fatty liver disease (NAFLD). Progression of simple steatosis to steatohepatitis (NASH) has been proposed by two hit hypothesis, the accumulation of lipid in the form of triglyceride as a first hit and oxidative stress leading to lipid peroxidation as a second hit which is needed for the development of NASH. But, emerging evidences from animal and human study points to metabolites of fatty acid as the real culprits in the hepatocellular injury in NASH. Increase free fatty acid release from adipose tissue to the liver, plays a key role in the onset of lipotoxic liver injury and progression. Ectopic fat accumulation in liver & muscle and subsequent activation of inflammation pathway causes cellular dysfunction. Cross talk between dysfunctional adipocytes and the liver recruits multiple cell population including macrophage and other immune cell. In this review, the role of lipotoxicity, fatty acid metabolites, inflammation, ER stress and genetic predisposition in the pathogenesis of NAFLD will be discussed.