Abstract
Non-alcoholic liver disease (NAFLD) constitutes a global health pandemic. It is estimated that about 25% of the world's population suffers from NAFLD. In the long-term, a subgroup of the patients can develop inflammation and fibrosis. The end result in some cases is cirrhosis and even liver-related death. The epidemiology and natural history of NAFLD lead to extreme financial costs.
Highlights
The diagnosis of non-alcoholic fatty liver disease (NAFLD) is based upon evidence of hepatic steatosis, either by imaging or by histology after the exclusion of other secondary causes of hepatic fat accumulation such as significant alcohol consumption, use of steatogenic medication and hereditary, autoimmune or viral hepatic disorders
NAFLD is histologically further categorized into non-alcoholic fatty liver (NAFL) defined as the presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes, and non-alcoholic steatohepatitis (NASH) defined as the presence of hepatic steatosis and inflammation with hepatocyte injury with or without fibrosis.[1]
Advanced fibrosis occurs in a subgroup of patients with NASH, leading to cirrhosis and possibly to the development of hepatocellular carcinoma.[2]
Summary
The diagnosis of non-alcoholic fatty liver disease (NAFLD) is based upon evidence of hepatic steatosis, either by imaging or by histology after the exclusion of other secondary causes of hepatic fat accumulation such as significant alcohol consumption, use of steatogenic medication and hereditary, autoimmune or viral hepatic disorders. The siRNA-mediated targeted knock down of S1P1 prevented the expression of TNF-α and MCP-1 in HEPG2 cells.[9] Subsequently, another experimental study of NAFLD, showed that sphingosine kinase 1 deficiency or siRNA-mediated knock down of S1P2 and S1P3 receptors protected animals from the development of steatosis.
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