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The amount and activity of placental enzymes, receptors, and transport proteins will determine the extent of lipid transfer to the fetus that strongly contributes to fetal fat accretion.Several studies have shown an association between the percentage of maternal plasma docosahexaenoic acid during gestation and the development of cognitive functions in the neonate. The functionality of the placenta could affect neonatal adiposity and fetal levels of long-chain polyunsaturated fatty acids in the offspring.Both in-vitro and human in-vivo studies using labeled fatty acids (FAs) reported a preferential placental–fetal transfer of long-chain polyunsaturated fatty acids, although the mechanisms are still uncertain. The placenta uptakes the maternal circulating nonesterified fatty acids (NEFAs) and FAs released by maternal lipoprotein lipase and endothelial lipase. These NEFAs enter the cell through passive diffusion or by membrane carrier proteins. NEFAs bind to cytosolic fatty-acid-binding proteins to interact with subcellular organelles, including the endoplasmic reticulum, mitochondria, lipid droplets and peroxisomes. Knowledge about FA metabolism and adaptations in response to obesity or diabetes in human placenta is more limited, and contradictory results are available in their influence on placental lipases and carriers.