Non-alcoholic fatty liver disease (NAFLD), the most common cause of chronic liver disease in Western countries, comprises a disease spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), advanced fibrosis and cirrhosis. Fatty liver develops when fatty acid uptake and de novo fatty acid synthesis exceed fatty acid oxidation and export as very low-density lipoprotein/triglycerides. Because of its high prevalence and its association with obesity, metabolic syndrome, type 2 diabetes, dyslipidaemia and hypertension, NAFLD has become an important public health problem. The pathogenesis of NAFLD has to date not been completely clarified. Research has been conducted regarding the role of insulin resistance, lipotoxicity, oxidative stress and chronic inflammation. Visceral adipose tissue has increasingly been recognised as a biologically active organ contributing to the pathogenesis of NAFLD. Its role in the development of fatty liver might be situated at several levels: as a source of free fatty acids, by the production of adipocytokines, as a cause of insulin resistance and by inflammation.
Soluble Molecules Released From Visceral Adipose Tissue May Contribute to the Development of Advanced Non-Alcoholic Fatty Liver Disease
