PROBIEN   20416
INSTITUTO DE INVESTIGACION Y DESARROLLO EN INGENIERIA DE PROCESOS, BIOTECNOLOGIA Y ENERGIAS ALTERNATIVAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Maternal fat overfeeding programs lack of response to lipid catabolism regulators in the livers of fetuses and offspring, possible implications for lipid overaccumulation
Autor/es:
WHITE, VERÓNICA; RADICE, MARTINA; JAWERBAUM, ALICIA; HEINECKE, FLORENCIA; JAWERBAUM, ALICIA; HEINECKE, FLORENCIA; MAZZUCCO, MARÍA BELÉN; MAZZUCCO, MARÍA BELÉN; WHITE, VERÓNICA; RADICE, MARTINA
Lugar:
Puerto Varas
Reunión:
Congreso; VII Latin American Symposium on Maternal Fetal Interaction and Placenta (SLIMP); 2017
Institución organizadora:
SLIMP
Resumen:
Leptin induces liver lipid catabolism, increasing acetyl CoA oxidase (ACO) andcarnitin palmitoyl transferase-1 (CPT1) expression, through peroxisome proliferator activated receptor a (PPARa) activation. We previously found liver lipid overaccumulation and no response to leptin-induced lipid catabolic actions in fetuses from rats fed with an overload of fat (SFD). Objective: to analyse whether fetuses and offspring from the SFD group respond to the lipid catabolic effects of the PPARa activator clofibrate. Methods: Female rats were fed with standard (controls) or saturated fat diet (28% fat) since they were 6 week-old (SFD rats). After 8 weeks, they were mated with control males. Control and SFD rats were euthanized at gestational day 21 or allowed to deliver and their offspring euthanized at 140 days of age. Offspring and fetal livers were cultured (3h) (n=6) with or without clofibrate (0.1m M). Lipid levels (triglycerides (TG), phospholipids (PL), free fatty acids (FA) and cholesteryl esters (CE)) were assessed by TLC. ACO and CPT1 expression was analysed by PCR. Results: In livers from control fetuses, clofibrate decreased lipid levels (females: TG, FA, and EC 25%, males: PL and FA 30%, P