Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1664
Peer-review started: June 27, 2015
First decision: July 20, 2015
Revised: August 20, 2015
Accepted: September 28, 2015
Article in press: September 30, 2015
Published online: January 28, 2016
Hepatic steatosis defined as lipid accumulation in hepatocytes is very frequently found in adults and obese adolescents in the Western World. Etiologically, obesity and associated insulin resistance or excess alcohol intake are the most frequent causes of hepatic steatosis. However, steatosis also often occurs with chronic hepatitis C virus (HCV) infection and is also found in rare but potentially life-threatening liver diseases of pregnancy. Clinical significance and outcome of hepatic triglyceride accumulation are highly dependent on etiology and histological pattern of steatosis. This review summarizes current concepts of pathophysiology of common causes of hepatic steatosis, including non-alcoholic fatty liver disease (NAFLD), alcoholic fatty liver disease, chronic HCV infections, drug-induced forms of hepatic steatosis, and acute fatty liver of pregnancy. Regarding the pathophysiology of NAFLD, this work focuses on the close correlation between insulin resistance and hepatic triglyceride accumulation, highlighting the potential harmful effects of systemic insulin resistance on hepatic metabolism of fatty acids on the one side and the role of lipid intermediates on insulin signalling on the other side. Current studies on lipid droplet morphogenesis have identified novel candidate proteins and enzymes in NAFLD.
Core tip: Fatty liver disease is a highly prevalent condition in the Western World. This article summarizes the most frequent causes and states of hepatic steatosis, including non-alcoholic fatty liver disease (NAFLD), alcoholic fatty liver, drug-induced forms, hepatitis C virus infections, and acute fatty liver of pregnancy. Important pathophysiological and cellular aspects of various forms of fatty liver disease are reviewed as well as the clinically relevant close interaction between hepatic triglyceride accumulation and insulin resistance in NAFLD.