Maternal saturated fat-enriched diet promotes leptin resistance in the fetal liver and programs lipid homeostasis impairment in the offspring

MARÍA BELEN MAZZUCCO; DAIANA FORNES; ALICIA JAWERBAUM; VERÓNICA WHITE

Mar del Plata

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

Maternal obesity leads to impaired metabolic programming. In a rat model of saturated fat overload in the maternal diet, we have previously found increased fetal liver lipid content. Lipid catabolism in the liver assures proper lipid homeostasis. Leptin regulates lipid catabolism in several tissues. Objective: To investigate whether an overload of saturated fat on the maternal diet impairs leptin effects on hepatic lipid catabolism in rat fetuses at term gestation and whether these anomalies are sustained in the offspring of these rats. Methods: Female Wistar rats were fed with a standard (5% fat) or with a saturated fat diet (28% fat) from 6 weeks of age (SFD rats). After 8 weeks of diet, they were mated with control males. Control and SFD rats were euthanized at 21 days of gestation and fetal livers obtained 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 130 days of age. Livers were analyzed for lipid accumulation (TLC) and acylCoA oxidase (ACO) expression (PCR). Results: Leptin induced a decrease in triglycerides (49%), free fatty acids (75%) and cholesteryl esters (42%) concentrations in fetal livers from control rats (p