CONICET | Buscador de Institutos y Recursos Humanos

Introduction: Fat overload in maternal diet can increase lipid transfer across the placenta to the developing fetus. This may cause fetal metabolic alterations and macrosomia. Placental endothelial (EL) and lipoprotein (LPL) lipases are key regulators of maternal-to-fetal lipid transport. The aims of this study were to evaluate the effects of fat overload in the diet of pregnant rats on maternal, fetal and placental weight, as well as leptin, insulin and lipid profile in maternal and fetal plasma, and to analyze placental expression of lipases, evaluating the role of leptin in the expression of EL and LPL. Methods: Rats were subjected to a standard diet (control) with 5% fat or a fatty diet (FD) enriched with 25% saturated fat. Also, fetuses from control rats were injected with leptin (200 ng) or vehicle through the uterine wall on days 19, 20 and 21 of gestation. Maternal plasma, placentas, fetuses and fetal plasma were obtained on day 21 of gestation. Plasma insulin and leptin levels were evaluated by EIA, lipid levels by colorimetric assays, and placental expression of EL and LPL by PCR. Results: Maternal weight gain, and fetal and placental weight were greater in FD group (p<0.05) compared to controls. The FD group showed higher triglycerides (p<0.01), insulin (p<0.05) and leptin (p<0.01) levels in maternal and fetal plasma. Also, FD fetuses had increased cholesterol plasma levels (p<0.01). Placentas from the FD group and from leptin-injected fetuses showed no changes in EL expression, but, interestingly, the same increase in LPL expression (p<0.05), when compared to controls. Conclusions: Fat overload in maternal diet causes an increase in fetal lipid and leptin levels, which promotes lipid transfer to the fetus by inducing placental LPL expression. Fetal and placental overgrowth can be caused by the increased bioavailability of insulin, leptin and lipids in the developing fetus.

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