Non-alcoholic fatty liver disease (NAFLD) is now the leading cause of chronic liver dysfunction in developed countries and is predominantly caused by obesity.
Its path ranges from steatosis (fat deposition in the liver), through fat with inflammation (non-alcoholic steatohepatitis, NASH), to NASH with reversible scarring (fibrosis), to cirrhosis (severe scarring) which may be irreversible.
Non-alcoholic fatty liver disease may progress through cirrhosis or other pathways to primary liver cancer (hepatocellular carcinoma, HCC). The rising rates of non-alcoholic fatty liver disease probably explain the rising rates of primary liver cancer.
The population prevalence of non-alcoholic fatty liver disease approaches 35% in some developed countries such as the USA, with the UK not far behind. Alarming rates of obesity, predicted to be 50% of the adult UK population within the next few decades makes it a major public health issue.
Non-alcoholic fatty liver disease induced liver injury leads to insulin resistance, in the presence or absence of type 2 diabetes, resulting in fat deposition in the liver which then causes increased oxidant stress, cell death and subsequent activation of scar-forming cells in the liver. There is at present no single diagnostic test for non-alcoholic fatty liver disease but a liver biopsy is often performed to accurately stage the disease and guide prognosis and treatment.
Emerging therapies include those which enhance insulin sensitivity, reduce metabolic risks or reduce activation of stellate cells (the predominant fibrogenic cells in the liver) or those which may enhance liver repair.
Such drugs are:
- Vitamin E
- Angiotensin receptor blockers
- Alpha -1 antagonists
- Rimonabant, a cannabinoid receptor type 1 antagonist also shows good promise in the treatment of NAFLD.