COMMENTARY
Fatty liver in chronic hepatitis C infection
Fatty liver in chronic hepatitis C infection: unravelling the mechanisms
1 University College London, Centre for Hepatology, Royal Free Hospital, London, UK; Guy’s and St Thomas’ Hospital, London, UK
2 Institute of Hepatology, University College London, London WC1 6BT, UK
Correspondence to:
Correspondence to:
Dr Jude A Oben
Centre for Hepatology, University College London, Royal Free Hospital, London NW3 2PF; jude.oben@gstt.nhs.uk
A step closer to understanding fatty liver due to HCV
| The first 150 words of the full text of this article appear below. |
Chronic hepatitis C virus (HCV) infection afflicts about 200 million people worldwide and is presently the most common cause of cirrhosis and hepatocellular carcinoma in Western countries. Over the last decade, an association between HCV infection, hepatic steatosis, insulin resistance (IR) and type II diabetes has been highlighted, although the cause–effect relationship underlying the co-existence of these phenomena has yet to be completely clarified.1 These observations are important because the presence of steatosis and/or IR in chronic HCV infection appears to modulate the progression of fibrosis and the response to antiviral therapy in chronic HCV infection.2–4
Mechanisms underling steatosis development in chronic HCV infection have been demonstrated to be genotype specific, with an apparent direct steatogenic effect of genotype 3, and an IR-associated steatosis effect exerted by genotype 1.5,6 The direct steatogenic effect of HCV genotype 3 is confirmed by findings such as
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Gut 2007 56: 1302-1308.[Abstract] [Full Text] [PDF]
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