الفهرس 
Childhood ObesityOnly 14 pages are availabe for public view
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Abstract
Nonalcoholic fatty liver disease (NAFLD) has emerged as the most common cause of chronic liver disease in pediatrics, affecting an alarming number (38%) of obese children. Its prevalence has more than doubled over the past 20 years, paralleling the increased prevalence of childhood obesity. NAFLD varies from steatosis to steatohepatitis to advanced fibrosis with cirrhosis. Children with NAFLD may develop end-stage liver disease with a consequent need for liver transplantation. As in adults, children with NAFLD have several metabolic impairments that increase the risk of developing of type 2 diabetes mellitus, the metabolic syndrome and cardiovascular disease. Evidence that not all of the obese patients develop NAFLD suggests that disease progression is likely to depend on complex interplay between environmental factors and genetic predisposition. A number of genes regulate a wide spectrum of mechanisms involved in NAFLD pathogenesis, including lipid accumulation into the liver, oxidative stress, inflammation, and fibrogenesis. Several common gene variants have been implicated in the pathogenesis of fatty liver disease. The most important is probably the patatin like phospholipase containing domain 3 gene (PNPLA3) discovered by the Hobbs’ group in 2008.