Non-alcoholic fatty liver disease pathogenesis: the present and the future.
Non-alcoholic fatty liver disease is the clinical hepatic expression of metabolic syndrome. The prevalence of non-alcoholic fatty liver disease is around 20-30%, and with a rapid increase in the metabolic risk factors in the general population, non-alcoholic fatty liver disease has become the most common cause of liver disease worldwide. A fraction (20-30%) of non-alcoholic fatty liver disease patients develop a potentially progressive hepatic disorder, namely non-alcoholic steatohepatitis, leading to end-stage liver disease. The pathogenesis of non-alcoholic fatty liver disease is not entirely understood, and even if insulin resistance is a major pathogenetic key, many other factors are implicated in both liver fat accumulation and disease progression to non-alcoholic steatohepatitis. In this review we aim to examine the literature, principally concerning human non-alcoholic fatty liver disease pathogenesis, and to identify the newest, most promising clinical and basic research data.
Petta
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Cattedra & Unità Operativa di Gastroenterologia, Di.Bi.M.I.S., University of Palermo, Palermo, Italy. petsa@inwind.it
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D054392:Adipokines / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004032:Diet; D018450:Disease Progression; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005234:Fatty Liver / Q000097:blood / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology*; D020022:Genetic Predisposition to Disease; D022781:Hepatocytes / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D008066:Lipolysis / Q000502:physiology; D008099:Liver / Q000737:chemistry; D008930:Mitochondria, Liver / Q000502:physiology; D018384:Oxidative Stress / Q000235:genetics; D012307:Risk Factors
D054392:Adipokines; D016207:Cytokines; D005230:Fatty Acids, Nonesterified