Published online Jun 8, 2015. doi: 10.4254/wjh.v7.i10.1337
Peer-review started: August 1, 2014
First decision: September 16, 2014
Revised: February 8, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: June 8, 2015
Processing time: 307 Days and 6.6 Hours
There is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in “pure” steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients.
Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory element-binding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements.