Lipid profile in intrauterine growth restriction

Reduction in the intrauterine supply of nutrients might lead to Intrauterine growth restriction alterations of the fetal growth trajectory that results in attainment of fetal own growth potential missed. IUGR is, together with premature delivery, the most relevant cause of perinatal mortality and morbidity, affecting approximately 7–15% of pregnancies. Although maternal, placental, and fetal causes may reduce the potential for fetal growth, no known causes can be detected in most cases of IUGR. These cases share a common placental phenotype, also called for many years “placental insufficiency.” In the last years many studies have described the vascular, metabolic, and endocrine changes occurring in IUGR, although the initiating factors are still to be understood. IUGR fetuses show a decreased deposition of tissue as a result of reduced uptake of nutrients from the umbilical circulation. In particular, the fetal fat component seems to be affected. Among nutrients, some fatty acids are particularly relevant for fetal nutrition and pregnancy outcome. In particular, the long chain polyunsaturated fatty acids (LCPUFA) of the n-3 and n-6 series, i.e., arachidonic acid (AA) and docosahexaenoic acid (DHA) need to be made available through the placenta since they cannot be synthesized in the fetus. They are important structural elements of cells guaranteeing the plasticity of the membranes; they are needed for the normal development of the central nervous system and retina. The biological roles of omega-3 and omega 6 FA involve eicosanoid metabolism, membrane properties, and regulation of gene expression. Significant changes in the ratios between the LCPUFA DHA and AA and their precursors ALA and LA have been reported in IUGR sampled at cordocentesis when compared to normally grown fetuses of similar gestational age. Altered availability of LCPUFA in preterm IUGR might have an important role in the increased brain damage susceptibility shown by these fetuses.