Pre-eclampsia (PET) is a multi-system disorder particular to pregnancy. It is characterised by widespread endothelial dysfunction, resulting in hypertension due to vasoconstriction, proteinuria attributable to glomerular damage and oedema secondary to increased vascular permeability. PET has a complex aetiology involving a spectrum of exaggerated disturbances in maternal metabolism, potentially resulting from a trigger from the placenta. PET shares many risk factors with cardiovascular disease (CVD) and may be associated with increased risk of future maternal CVD. The similarities between the metabolic syndrome and PET, has lead to the proposal that PET is metabolic syndrome of pregnancy. It is likely that a combination of environmental, genetic and metabolic parameters have a role in the aetiology of PET, rather than one specific factor. Although there are abundant data on the metabolic pathways and vascular function in the non-pregnant individual, there are little such data with respect to pregnancy and PET. The purpose of this thesis was to concentrate on PET as a metabolic disorder and to focus on the key mediators involved in the metabolic syndrome including PPAR receptors, lipoprotein metabolism, insulin resistance and inflammation. PPARs are a family of nuclear receptors controlling pathways involved in the metabolic syndrome including adipocyte differentiation, glucose and lipid homeostasis and fatty acid metabolism. Animal and human models have highlighted a role for the PPARs in pregnancy. In this thesis, the placental localisation and expression of each of the PPARs (alpha, delta and gamma) were determined, in uncomplicated and PET and 1UGR pregnancy.