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Journal of Lipid Research, Vol. 46, 2405-2414, November 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Lipoprotein metabolism of pregnant women is associated with both their genetic polymorphisms and those of their newborn children¹

Olivier S. Descamps^2,*,,, Monique Bruniaux, Pierre-Francois Guilmot^**, René Tonglet^1,* and Francis R. Heller

^* Epidemiology Unit, School of Public Health, Université Catholique de Louvain, Brussels, Belgium
Center for Medical Research at Jolimont, Centre Hospitalier Jolimont-Lobbes, Haine Saint-Paul, Belgium
Department of Internal Medicine, Centre Hospitalier Jolimont-Lobbes, Haine Saint-Paul, Belgium
^** Department of Obstetrics and Gynecology, Centre Hospitalier Jolimont-Lobbes, Haine Saint-Paul, Belgium

¹ The authors acknowledge the help and encouragement of Dr. René Tonglet, who died during the course of these investigations.

Published, JLR Papers in Press, August 16, 2005. DOI 10.1194/jlr.M500223-JLR200

² To whom correspondence should be addressed. e-mail: descaoli{at}skynet.be

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 < 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).

Supplementary key words low density lipoprotein • high density lipoprotein • fetus • pregnancy • placenta

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