Fatty liver disease begins as a simple build-up of fat in the liver. In some cases this fat may not cause any problems, in others it can cause the liver to become inflamed (swollen) eventually leading to the development of scar tissue (cirrhosis). In its most severe form, fatty liver disease can result in liver cancer or liver failure.
The two main contributers to fatty liver disease are poor nutrition (linked to obesity) and alcohol consumption. An estimated 75 per cent of obese individuals are at risk of developing a simple fatty liver and up to 23 per cent are at risk of developing fatty liver with inflammation.
It is not clear why some people with fat in their liver progress to liver cancer and why some do not. Funded by a CLF graduate studentship grant, Michael Ryczko and his colleagues (Mount Sinai Hospital, Ontario) are trying to determine what roles genetics and metabolism (or nature vs. nurture) play in the development of liver cancer. The project is focusing on the impact of a high-fat diet and the effect of a particular gene called Mgat5, which is often found to be more active in cancerous tumours (including those in the liver) and correlates to disease progression. Better understanding of what happens at the molecular level in obesity-related liver cancer, may lead to the identification of a biomarker that could help pinpoint who may develop liver cancer.