Published online Jun 21, 2014. doi: 10.3748/wjg.v20.i23.7347
Revised: January 4, 2014
Accepted: January 20, 2014
Published online: June 21, 2014
Processing time: 255 Days and 15.4 Hours
Non-alcoholic fatty liver disease (NAFLD) comprehends a wide range of conditions, encompassing from fatty liver or steatohepatitis with or without fibrosis, to cirrhosis and its complications. NAFLD has become the most common form of liver disease in childhood as its prevalence has more than doubled over the past 20 years, paralleling the increased prevalence of childhood obesity. It currently affects between 3% and 11% of the pediatric population reaching the rate of 46% among overweight and obese children and adolescents. The prevalence of hepatic steatosis varies among different ethnic groups. The ethnic group with the highest prevalence is the Hispanic one followed by the Caucasian and the African-American. This evidence suggests that there is a strong genetic background in the predisposition to fatty liver. In fact, since 2008 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. This article reviews the current knowledge regarding the role of ethnicity and genetics in pathogenesis of pediatric fatty liver.
Core tip: The prevalence of hepatic steatosis varies among different ethnic groups. Ethnicity with the greatest prevalence of non-alcoholic fatty liver disease (NAFLD) is the Hispanic one followed by Caucasian and then African-Americans. NAFLD exhibits tight links with insulin resistance and metabolic syndrome. Several gene variants have been so far identified by Genome Wide Association Studies or by a candidate gene approach as associated with fatty liver disease. The PNPLA3 rs738409 and the GCKR rs1260326 are the strongest variants associated with fatty liver in paediatrics.