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Abstract

During gestation, the increase in maternal body mass mainly corresponds to lipid stores which are synthesized during the first two thirds of pregnancy. This is related to maternal hyperphagia and is a consequence of enhanced lipogenesis in adipose tissue. During the last third of gestation, lipid metabolism switches to a catabolic condition with net fat breakdown and enhanced plasma levels of both free fatty acids FFA and glycerol. Placental transfer of these compounds is low and they are driven to maternal liver where they are used for triglyceride synthesis, or FFA for the synthesis of ketone bodies and glycerol for gluconeogenesis. All these pathways are enhanced during late gestation, although ketogenesis is only enhanced under fasting conditions. Enhanced liver VLDL-triglycerides production in the presence of decreased extrahepatic lipoprotein lipase (LPL), is responsible for the increase of VLDL-triglycerides in maternal plasma. This, together with enhanced chofesterol ester transfer protein activity is responsible
for the increase of triglycerides in lipoproteins of higher density, LDL and HDL. In spite of the imperrneability of the placenta to triglycerides, such hypertriglyceridemia benefits the fetus and the newborn in several ways: 1) Under fasting conditions, maternal liver shows enhanced LPL activity which allows the u take of circulating triglycerides by this organ and their use as substrates for ketogenesis; 2) The presence
of lipase activities in the placenta allows essential fatty acids of maternal plasma triglycerides to become available to the fetus; and 3) The induction of LPL in mammary gland around parturition drives plasma triglycerides to this organ for milk synthesis in preparation to lactation. Although certain deviations of maternal hyperlipidemia may affect fetal growth, the development of maternal hypercholesterolemia does not have negative effects to the fetus, probably as a consequence of the lack of placental cholesterol transfer.