title: Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas.
abstract: Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P<0.01) in mothers and fetuses, an increase in maternal (P<0.05) and fetal weight (P<0.01), overaccumulation of lipids in fetal liver (P<0.01), and enhanced leptin expression in the placenta and fetal liver (P<0.05). Placental expression of IR and LPL was increased (P<0.05), and ObR decreased (P<0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P<0.05) and upregulation of LPL expression (P<0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects.
authors.affiliation: Laboratory of Reproduction and Metabolism, School of Medicine, Center for Pharmacological and Botanical Studies, CEFyBO-CONICET, University of Buenos Aires, Paraguay 2155 17th floor CABA 1121, Buenos Aires, Argentina.
authors.forename: M B
authors.initials: MB
authors.lastname: Mazzucco
authors.forename: R
authors.initials: R
authors.lastname: Higa
authors.forename: E
authors.initials: E
authors.lastname: Capobianco
authors.forename: M
authors.initials: M
authors.lastname: Kurtz
authors.forename: A
authors.initials: A
authors.lastname: Jawerbaum
authors.forename: V
authors.initials: V
authors.lastname: White
mesh_terms: D000818:Animals; D059305:Diet, High-Fat; D004041:Dietary Fats / Q000378:metabolism / Q000494:pharmacology; D005227:Fatty Acids / Q000494:pharmacology*; D005260:Female; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008049:Lipase / Q000235:genetics / Q000378:metabolism; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D010920:Placenta / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D054411:Receptors, Leptin / Q000235:genetics / Q000378:metabolism*
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids; D020738:Leptin; D008055:Lipids; D054411:Receptors, Leptin; D011972:Receptor, Insulin; D008049:Lipase; C498742:Lipg protein, rat; D008071:Lipoprotein Lipase