Implications of dietary fatty acids during pregnancy on placental, fetal and postnatal development: a review.

Abstract

During pregnancy, the mother adapts her metabolism to support the continuous draining of substrates by the fetus. Her increase in net body weight (free of the conceptus) corresponds to the accumulation of fat depots during the first two-thirds of gestation, switching to an accelerated breakdown of these during the last trimester. Under fasting conditions, adipose tissue lipolytic activity is highly enhanced, and its products, free fatty acids (FF A) and glycerol, arc mainly driven to maternal liver, where FF A are converted to ketone bodies and glycerol to glucose, which easily cross the placenta and sustain fetal metabolism. Lipolytic products reaching maternal liver are also used for triglyceride synthesis that are released in turn to the circulation, where together with an enhanced transfer of triglycerides among the different lipoprotein fractions, and a decrease in cxtrahepatic lipoprotein lipase activity, increase the content of triglycerides in all the lipoprotein fractions. Long chain polyunsaturated fatty acids (LCPUFA) circulate in maternal plasma associated to lipoprotein triglycerides, and in a minor proportion in the form of FF A. Despite the lack of a direct placental transfer of triglycerides, diffusion of their fatty acids to the fetus is ensured by means of lipoprotein receptors, lipoprotcin lipase activity and intracellular lipase activities in the placenta. Maternal plasma FF A are also an important source of LCPUF A to the fetus, and their placental uptake occurs via a selective process of facilitated membrane translocation involving a plasma membrane fatty acid-binding protein. This mechanism together with a selective cellular metabolism determine the actual rate of placental transfer and its selectivity, resulting even in an enrichment of certain LCPUF A in fetal circulation as compared to maternal. The degree to which the fetus is capable of fatty acid desaturation and elongation is not clear, although both term and preterm infants can synthesize LCPUF A from parental essential fatty acids. Nutritional status of the mother during gestation is related to fetal growth, and excessive dietary intake of certain LCPUFA has inhibitory effects on A-5- and A-6-desaturases. This inhibition causes major declines in arachidonic acid levels, as directly found in pregnant and lactating rats fed a fish oil-rich diet as compared to olive oil. An excess in dietary PUF A may also enhance peroxidation and reduce antioxidant capacity. Thus, since benefit to risks of modifying maternal fat intake in pregnancy and lactation arc not yet completely established, additional studies are needed before recommendations to increase LCPUF A intake in pregnancy are made.