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Increased placental fatty acid transporter 6 and binding protein 3 expression and fetal liver lipid accumulation in a mouse model of obesity in pregnancy.

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AJP Regulatory Integrative and Comparative Physiology

Published online on

Abstract

Obesity in pregnancy is associated with increased fetal growth and adiposity, which, in part, is determined by transplacental nutrient supply. Trophoblast uptake and intracellular trafficking of lipids are dependent on placental fatty acid transport proteins (FATP), translocase (FAT/CD36) and fatty acid binding proteins (FABP). We hypothesized that maternal obesity in mice leads to increased placental expression of FAT/CD36, FATPs and FABPs, and lipid accumulation in the fetal liver. C57/BL6J female mice were fed either a control (C; n=10) or an obesogenic (OB; n=10) high fat-high sugar diet before mating and throughout pregnancy. At E18.5 placentas and fetal livers were collected. Trophoblast plasma membranes (TPM) were isolated from placental homogenates. Expression of FAT/CD36 and FATP (TPM) and FABP (homogenates) was determined by immunoblotting. Gene expression was assessed by RT-qPCR. Sections of fetal livers were stained for Red Oil O and lipid droplets were quantified. TPM protein expression of FAT/CD36, FATP 2 and 4 was comparable between C and OB groups. Conversely, TPM FATP 6 expression was increased by 35% in OB compared to C placentas without changes in mRNA expression. FABP 1, 3-5 and PPAR were expressed in homogenates and FABP 3 expression increased 27% in OB compared to C placentas; however no changes were observed in mRNA expression. Lipid droplet accumulation was 10-fold higher in the livers of fetuses from OB compared to C group. We propose that increased lipid transport capacity in obese mice promotes transplacental fatty acid transport and contributes to excess lipid accumulation in the fetal liver.