Hyperlipidemia and vitamin E metabolism in pregnancy.

Abstract

Fat accumulation during pregnancy as result of both hypcrphagia and increased lipid synthesis takes place during the first two-thirds of gestation, whereas it declines during the last third. as a consequence of enhanced adipose tissue lipolysis. This change together with a decrease in adipose tissue lipoprotein lipase (LPL) activity causes a net enhanced breakdown of fat stores, which is facilitated by the insulin-resistant condition that is normally present during late pregnancy. The main fate of the lipolytic products is maternal liver. where they arc re-esterified for the synthesis of triacylglycerols (TG), which are released into the circulation as part of very low density lipoproteins (VLDL). The abundance of VLDL-TG in the presence of an increase in cholesteryl ester transfer protein activity taking place at mid gestation contribute to the accumulation ofTG in the lipoprotcin fractions of higher density, LDL and HDL. Maternal hyperlipidemia is associated with the predominance of small and dense LDL-particlcs, which arc more susceptible to oxidation. The higher levels of lipid peroxides during late pregnancy arc accompanied by higher levels of vitamin E, which values correlate with maternal hyperlipidemia. Although the lipolytic activity of LPL seems to play a significant role in the uptake of u-tocopherol in certain tissues, like mammary gland around parturition, this is not the case in others, where LPL may function as a cell surface proteoglycananchored bridge for lipoprotcins, facilitating the uptake of LDL a-tocophcrol. Other mechanisms exist for the tissue uptake of a-tocophcrol, including the receptor-mediated lipoproti:in cndocytosis, the LDL receptor pathway or the scavenger receptor class B type I. The ATP-binding cassette transporter A I has been also implicated in the supply of utocopherol in the feto-matemal unit. Despite that the a-tocopherol transfer protein seems to act in conjunction with lipoprotein receptors, lipolytic enzymes and fatty acid binding proteins in the placenta to facilitate the transfer of a-tocopherol between maternal and feta) circulation, its rate is very low, justifying the low levels of vitamin E in tetal plasma. The induction of LPL activity in mammary gland around parturition contribute to both the disappearance of maternal hyperlipidemia and the efficient uptake by mammary gland of circulating u-tocopherol, allowing its availability in the suckling newborn.