Evidence suggests that altered maternal nutrition increases susceptibility to the metabolic syndrome in adult offspring. An increase in the prevalence of metabolic syndrome has been linked to an increase in incidence of non-alcoholic fatty liver disease (NAFLD), which can range from fatty liver (steatosis), to non-alcoholic steatohepatitis (NASH) and fibrosis. Since mitochondrial dysfunction impairs fatty liver homeostasis, increases reactive oxygen species and triggers lipid peroxidation mitochondrial dysfunction it is a likely candidate for NAFLD disease progression. To investigate the effect of maternal nutrition on mitochondrial dysfunction and development of NASH, we determined changes in electron transport chain (ETC) enzyme complex activity in liver tissue from mouse offspring that were exposed to a high fat or control diet both pre and post-natally Female C57 BL/6J black mice were randomly assigned to either a high fat diet (HF- 45% kcal fat, 20% kcal protein, 35% kcal carbohydrate, n =10) or standard laboratory chow diet (C- 21% kcal fat, 18% kcal protein, 63% kcal carbohydrate, n = 10). Dams were fed 4 weeks prior to conception, during gestation and lactation. At weaning the offspring were assigned either HF or C diet, generating 4 experimental groups: HF/HF (n= 12), HF/C (n = 12), C/HF (n = 12), C/C (n = 12), which represents prenatal/postnatal diet respectively. Offspring food intake and weights were recorded at weekly intervals. Locomotor activity and blood pressure was measured at 13 weeks of age. At 15 weeks offspring were killed and tissues were weighed and collected. Hepatic mitochondrial complex (I, II/III, and IV) activity was measured by spectrophotometer following addition of relevant cofactors (rotenone, antimycin reduced cytochrome c respectively). Results were standardized using citrate synthetase activity. Histological analysis of liver specimens stained with haematoxylin and eosin (H and E) were used to determine levels of steatosis. In liver tissue from both the HF/C and HF/HF offspring mitochondrial complex I, II/III and IV activity was significantly reduced when compared to both the C/C and C/HF (p < 0.05) groups. The greatest decrease was observed with Complex I, where a 3.2 and 3.7-fold reduction in activity levels were seen HF/HF offspring (p < 0.05) and HF/C offspring (p < 0.05) respectively, compared to C/C offspring. This data implies that the pre-natal exposure to a HF diet impairs complex activity and mitochondrial function. Steatosis was visible in liver sections from C/HF and HF/HF animals, and there was an inflammatory infiltrate in sections from the HF/HF group. This data provides preliminary evidence to suggest that exposure to a HF diet in utero may contribute to disease progression of NASH.