Fat overload in maternal diet induces pro-inflammatory and oxidative alterations in placenta and fetal liver from rats.

MB MAZZUCCO, D FORNES, A JAWERBAUM AND V WHITE

Workshop; International Postgraduate Workshop on Pregnancy Diseases (IPW) 2012. Vascular Dysfunction Mechanisms.; 2012

Fat overload in maternal diet induces metabolic disturbances in the mother and fetus. Increased levels of tissue and circulating lipids define a pro-inflammatory and hyperlipidemic intrauterine environment. We developed a rat model in which an increase of 25% saturated fat in the maternal diet generates placentomegaly, macrosomia, hyperlipidemia and fetal liver lipid overaccumulation. Mothers and fetuses have also increased levels of leptin, a hormone involved in lipid homeostasis, linked to pro-inflammatory pathways and modulation in nitric oxide (NO) production. Aims: We aimed to evaluate the expression of leptin receptor (OBR), lipid peroxidation and nitric oxide production (NO) in fetal liver and placenta from pregnant rats fed with a diet enriched in saturated fat. Methods: Wistar rats fed a standard diet (SD) or a diet supplemented with 25% saturated fats (DG) from 7 weeks of age, were mated with healthy males. At day 21 of pregnancy mothers and fetuses were sacrificed, placentas and fetal livers were removed and kept for the analysis of OBR by PCR, western-blot and immunohistochemistry. Lipid peroxidation and NO production were assessed by TBARS and nitrates-nitrites levels (Griess).Results: Placentas and fetal liver from DG group showed an increase in lipid peroxidation and NO production. The DG group also showed alterations in ObR gene and protein expression and localization in both placenta and fetal liver. Conclusions: DG induced pro-inflammatory and oxidative alterations in placenta and fetus that can be related to an excess of circulating lipids, possibly promoted by an increase in leptin actions.