More glucose crosses the placenta than any other substrate, but correlations between its concentration in maternal
plasma and fetal growth are not found consistently. The accumulation of maternal fat depots and hyperlipidemia are
the two principal changes in lipid metabolism during pregnancy. Although lipids cross the placenta with difficulty, maternal
plasma triacylglycerols (TAG) and non-esterified fatty acids (NEFA) correlate with fetal lipids, fetal growth and fat
mass under certain conditions. In intrauterine growth restriction, impaired placental transfer of lipophilic compounds
(long-chain polyunsaturated fatty acids and lipophilic vitamins) seems to underpin metabolic dysfunction and decreased
birth weight. In gestational diabetes mellitus (GDM), maternal TAG and NEFA levels correlate with neonatal anthropometric
measures. In GDM, adipocyte fatty acid-binding protein in fetuses correlated with neonatal fat mass; changes in
maternal or cord blood leptin, retinol binding protein 4 and adiponectin concentrations have been related to neonatal fat
mass or birth weight, although their importance remains to be investigated. The angiopoietin-like protein 4 (ANGPTL-4)
is secreted from adipose tissue, liver and placenta, and irreversibly inhibits lipoprotein lipase (LPL) activity. Maternal
plasma ANGPTL-4 is decreased in GDM, and it has been proposed to be responsible for an increase in placental LPL activity,
which would facilitate a greater fatty acid placental transfer, contributing to the higher fetal fat accumulation. Thus,
while evidence suggesting major involvement of maternal lipid metabolism in fetal adiposity and growth exists, the precise
mechanisms remain to be elucidated.
Adipocytokines, adipose tissue, gestational diabetes mellitus, hyperlipidemia, intrauterine growth restriction, nonesterified
fatty acids, placenta, pregnancy.
Universidad San Pablo CEU, Ctra. Boadilla del Monte km 5.3, 28668 Madrid, Spain.