Non Alcoholic Fatty Liver Disease (NAFLD) has become common liver disease in western countries. There is accumulating evidence that mitochondria play a key role in NAFLD. Nevertheless, the mitochondrial consequences of steatohepatitis are still unknown. The bioenergetic changes induced in a methionine-choline deficient diet (MCDD) model of steatohepatitis were studied in rats. Liver mitochondria from MCDD rats exhibited a higher rate of oxidative phosphorylation with various substrates, a rise in cytochrome oxidase (COX) activity and an increased content in cytochromes aa3. This higher oxidative activity was associated with a low efficiency of the oxidative phosphorylation (ATP/O i.e. number of ATP synthesized per natomO consumed). Addition of low concentration of cyanide, a specific COX inhibitor, restored the efficiency of mitochondria from MCDD rats back to the control level. Further, the relation between JO2 and protonmotive force ( p) (in non-phosphorylating state) was shifted to the left in mitochondria from MCDD rats, with or without cyanide. These results indicated that in MCDD rats, mitochondrial ATP synthesis efficiency was decreased in relation to both proton pump slipping at the COX level and increased proton leak although the relative contribution of each phenomenon could not be discriminated. MCDD mitochondria also showed a low reactive oxygen species production and a high lipid oxidation potential. We conclude that in MCDD-fed rats, liver mitochondria exhibit an energy wastage that may contribute to limit steatosis and oxidative stress in this model of steatohepatitis.