Published online Jul 21, 2014. doi: 10.3748/wjg.v20.i27.9072
Revised: March 20, 2014
Accepted: May 12, 2014
Published online: July 21, 2014
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease that might affect up to one-third of the adult population in industrialised countries. NAFLD incorporates histologically and clinically different non-alcoholic entities; fatty liver (NAFL, steatosis hepatis) and steatohepatitis (NASH-characterised by hepatocyte ballooning and lobular inflammation ± fibrosis) might progress to cirrhosis and rarely to hepatocellular cancer. NAFL increasingly affects children (paediatric prevalence is 4.2%-9.6%). Type 2 diabetes mellitus (T2DM), insulin resistance (IR), obesity, metabolic syndrome and NAFLD are particularly closely related. Increased hepatic lipid storage is an early abnormality in insulin resistant women with a history of gestational diabetes mellitus. The accumulation of triacylglycerols in hepatocytes is predominantly derived from the plasma nonesterified fatty acid pool supplied largely by the adipose tissue. A few NAFLD susceptibility gene variants are associated with progressive liver disease, IR, T2DM and a higher risk for hepatocellular carcinoma. Although not approved, pharmacological approaches might be considered in NASH patients.
Core tip: In this review article, non-alcoholic fatty liver disease (NAFLD) spectrum disease is discussed in detail. The epidemiology of NAFLD/nonalcoholic steatohepatitis and the relationship of NAFLD to different forms of diabetes mellitus including type 2 diabetes mellitus and gestational diabetes mellitus are reviewed. Attention is paid to the main biochemical events, to dysfunctional adipose tissue and visceral adiposity associated with NAFLD and insulin resistance, to mitochondrial dysfunction and to the role of the entero-insular axis in NAFLD. Genetics and potential pharmacological approaches are discussed.