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To explore whether the placenta contributes to the lipoprotein metabolism of pregnant women, we took advantage of the fact that placental proteins are encoded from the fetal genome and examined the associations between lipids of 525 pregnant women and the presence, in their newborns, of genetic polymorphisms of LPL and apolipoprotein E (APOE), two genes expressed in placenta. After adjustment for maternal polymorphisms, newborn LPL*S447X was associated with lower triglycerides ( ؊ 21 ؎ 9 mg/dl), lower LDL-cholesterol (LDL-C; ؊ 12 ؎ 5 mg/dl), lower apoB ( ؊ 14 ؎ 4 mg/dl), higher HDL-C (5 ؎ 2 mg/dl), and higher apoA-I (9 ؎ 4 mg/dl) in their mothers; newborn LPL*N291S was associated with higher maternal triglycerides (114 ؎ 31 mg/dl); and newborn APOE*E2 (compared to E3E3) was associated with higher maternal LDL-C (14 ؎ 6 mg/dl) and higher maternal apoB (14 ؎ 5 mg/dl). These associations (all P Ͻ 0.05) were independent of polymorphisms carried by the mothers and of lipid concentrations in newborns and were similar in amplitude to the associations between maternal polymorphisms and maternal lipids.Such findings support the active role of placental LPL and APOE in the metabolism of maternal lipoproteins and suggest that fetal genes may modulate the risk for problems related to maternal dyslipidemia (preeclampsia, pancreatitis, and future cardiovascular disease). -Descamps, O. S., M. Bruniaux, P-F. Guilmot, R. Tonglet, and F. R.

BackgroundLow weight at birth is associated with obesity in later life. One hypothesis to explain such an association is that genetic variants that increase the risk of obesity also reduce fetal weight. Recently, obesity in adults was found to be associated with common variants of the fat mass and obesity-associated (FTO) gene. We examined the association between FTO polymorphisms and birth weight in a singleton, full-term birth cohort of 494 newborn-mother pairs without any complications.ResultsThe risk alleles for obesity (“A” allele for the rs9939609 FTO variant and “G” allele for the rs9930506 FTO variant) were associated with low weight at birth. The mean differences per risk allele were −79 g (95% CI: −129 to −30; p = 0.002) for rs9939609 and −84 g (95% CI: −131 to −36; P < 0.001) for rs9930506. The level of association remained statistically significant after adjustment for the maternal risk allele and for variables usually associated with birth weight (−50 g, 95% CI: −99 to 0; p = 0.05 for rs9939609 and −48 g, 95% CI: −100 to 0; p = 0.05 for rs9930506). In the follow-up, the allelic difference in weight was attenuated over time.ConclusionsThe FTO variants that confer a predisposition to obesity later in life appear to be associated with low weight at birth. This finding favors the hypothesis of a common genetic denominator that predisposes to a low weight at birth and obesity in adults.

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