The obesity epidemic has resulted in an increase in the number of women entering pregnancy overweight or obese range (1). We have previously shown that exposure to maternal obesity in the periconceptional (PC) alone resulted in increased adiposity in female lambs (2). Maternal obesity both before and throughout pregnancy has been shown to result in alterations in hepatic fatty acid (FA) oxidation and lipogenesis, which are characteristic of non-alcoholic fatty liver disease (3-5). This has led to interest in understanding the type of dietary interventions before and during pregnancy, which may lead to optimal outcomes for the mother and offspring (1). Our aim was to determine the impact of exposure to maternal obesity or weight loss around conception in sheep on programming of molecules involved in hepatic FA oxidation and de novo lipogenesis in male and female lambs at 4 months of age. Donor ewes were allocated to 1 of 4 groups & fed the following diets in the PC period: 100% metabolisable energy requirements (MER) for ≥ 20wks (CC); 100% MER for ≥ 16wks & then 70% MER for 4wks (CR); ~180% MER for ≥ 20wks (HH); ~180% MER for ≥ 16wks & then 70% MER for 4wks (HR). This continued for 1wk post-conception before single embryos were transferred into recipient ewes of normal weight. At 16wks after birth, liver samples were collected to determine gene expression (qRT-PCR) and protein abundance (Western Blotting) of molecules regulating hepatic FA oxidation and synthesis. The effects of PC nutrition and sex were determined using a two-way ANOVA. A Duncan’s post hoc test was used to determine significant differences between groups. HH lambs had decreased gene expression and protein abundance of PPARα and a parallel decrease in PGC1α abundance (P<0.05). These lambs also had increased SIRT1 and decreased GCN5 abundance (P<0.05). Hepatic AMPKα1, AMPKα2 and SREBP1 was also increased (P<0.05) in these lambs. Exposure to maternal weight loss in obese ewes did not abolish all of the effects of maternal obesity on gene expression and protein abundance of these molecules. Furthermore, there was decreased (P<0.05) hepatic PGC1α and GCN5 abundance as well as increased (P<0.05) AMPKα2 abundance in CR lambs. We have shown that exposure to maternal obesity in the PC period programs potentially irreversible changes in hepatic lipid metabolism that persist in later life. We have also shown that dietary restriction in obese ewes in unable to abolish all of the effects of maternal obesity. Exposure of both normal weight and obese ewes to moderate dietary restriction resulted in an additional suite of changes within the liver. This highlights that there is vulnerability in offspring after exposure to periconceptional undernutrition to dysregulated hepatic lipid metabolism.