Adipose tissue is currently considered to be a metabolically active organ that secretes hormones which regulate energy balance. Leptin and adiponectin are its main metabolic products and have been implicated in a wide spectrum of human diseases including liver diseases. These two hormones have been initially studied in non-alcoholic fatty liver disease, which is considered to be part of the metabolic syndrome. Leptin seems to have fibrogenic potential and serum leptin levels have been found to be higher in patients with non-alcoholic steatohepatitis (NASH) than in controls. On the other hand, serum adiponectin levels have been found to be inversely related to the presence of NASH. As steatosis is a common histopathological finding of chronic hepatitis C, serum leptin and adiponectin levels were measured in such patients and found to be significantly higher and lower compared in healthy controls, respectively. However, it is not yet clear whether they are just markers of liver steatosis and fibrosis or whether they have a direct pathogenic or protective role. Therefore, the associations between leptin-adiponectin and liver steatosis and/or fibrosis should be evaluated further in prospectively designed studies including larger cohorts of NASH and chronic hepatitis C patients with detailed assessment of metabolic and several potential confounding factors. Moreover, their measurement in other liver diseases, which are considered to be infrequently associated with steatosis, such as chronic hepatitis B, would clarify if their action is mediated by or is independent of steatosis.