Fat overload in maternal diet and its impact on the offspring: possible implications in liver function

VERÓNICA WHITE; MARÍA BELEN MAZZUCCO; ALICIA JAWERBAUM

Mar del Plata

Congreso; VI Latin American Symposium on Maternal Fetal Interaction and Placenta (SLIMP); 2015

We aimed to analyze whether an overload of saturated fat in the maternal diet induces impairments in leptin-induced liver lipid catabolism that persist in the offspring´s later life, causing tissue damage and potential failure in liver function. Methods: Female Wistar rats were fed with a standard (5% fat) or a saturated fat diet (28% fat) from 6 weeks of age (SFD rats). After 8 weeks of diet, rats were mated with control males. Control and SFD rats were euthanized at 21 days of gestation and fetal livers obtained and preserved or prepared for further culture of explants (3h) with or without leptin (100 ng/ml). Another group of control and SFD rats were allowed to deliver, and their offspring euthanized at 21 or 140 days of age. Lipid metabolism: Livers from the offspring and incubated fetal livers were analyzed for lipid accumulation (TLC) and lipid catabolism enzymes (acetyl-CoA-carboxylase (ACO) and carnitin-palmitoyl-tranferase-1(CPT1)) expression (PCR). Tissue damage: Fetal and offspring livers were analyzed for oxidative stress markers, lipoperoxidation (TBARS) and nitric oxide production (nitrates/nitrites Griess) and specialized detoxifying channels (multidrugresistance-associated-protein 2 and 4 (MRP2 and MRP4)) expression(PCR). Results: Livers from SFD fetuses showed an increase in TBARS and nitrates/nitrites levels and diminished expression of ACO, CPT1, MRP2 and MRP4 (p