IntroductionPreeclampsia is a serious obstetric complication and a major cause of maternal and perinatal mortality and its pathogenesis is still unclear. We and other researchers have proven that long-chain Fatty Acid Oxidation (FAO) is associated with some forms of preeclampsia.Most fatty acids in the human body are long-chain fatty acids. The β-oxidation of fatty acids occurs in the mitochondria. After activation of long-chain fatty acids, they need assistance from carnitine as a carrier and catalysis of carnitine palmitoyltransferase I (CPT I) in the outer mitochondrial membrane and carnitine palmitoyltransferase II (CPT II) in the inner mitochondrial membrane to enter into the mitochondria [1]. Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) is a component of the mitochondrial trifunctional protein and is capable of catalyzing the third step of β-oxidation [2]. So CPT I, CPT II and LCHAD are key enzymes in the long-chain FAO process, and defects or dysfunction of which can result in disorders in longchain fatty acid transport into the mitochondria or oxidation, further resulting in inefficient energy release from FAO and affecting cell function.In a normal pregnancy, prolactin and estrogen increase the activity of hormone sensitive lipase, resulting in increased fat mobilization, increased maternal plasma Free Fatty Acids (FFA) and increased hepatic uptake of fatty acids. In the past, FAO was generally considered unimportant in placental and fetal development; however, a recent study found that this was not the case. Shekhawat et al. found that LCHAD and six other fatty acid β-oxidation enzymes were abundantly expressed in the placenta, indicating the long-chain FAO played an important role in placental development and energy supply [3]. Oey et al. found Very Long Chain Acyl-Coenzyme a Dehydrogenase (VLCAD) and LCHAD mRNA highly expressed during different stages in the embryo and fetal heart, liver and other tissues, and there were strong VLCAD, LCHAD and CPT II enzyme activities [4]. So long-chain FAO exists not only in the placenta, but also in embryonic tissues, and plays an important role in early development of the fetus. Thus, in a normal pregnancy placental and fetal development also requires FAO as an energy supply.Previous studies have found that LCHAD was associated with some forms of preeclampsia. Bartha and colleagues reported that LCHAD mRNA expression decreased in the placenta of preeclampsia patients compared with controls, and that the FAO ability of the placenta in preeclampsia patients was reduced [5]. Robinson et al. found that the plasma of preeclampsia patients could lead to lipid droplet aggregation in cultured human umbilical vein endothelial cells and decreased mitochondrial dehydrogenase activity [6]. In our previous studies we also found LCHAD expression decreased in the placenta with earlyonset severe preeclampsia, but there was no significant difference between late-onset preeclampsia and the control groups [7]. In animal experiments, we found that LCHAD expression was signifi...