Maternal fat overfeeding programs lack of response to lipid catabolism regulators in the livers of foetuses and offspring, possible implications for lipid overaccumulation

HEINECKE FLORENCIA; RADICE MARTINA; MAZZUCCO MARÍA BELÉN; ALICIA JAWERBAUM; WHITE VERÓNICA

Puerto Varas

Congreso; VII Latin American Symposium on Maternal Fetal Interaction and Placenta (SLIMP); 2017

SLIMP

Leptin induces liver lipid catabolism, increasing acetyl CoA oxidase (ACO)and carnitin palmitoyl transferase-1 (CPT1) expression, through peroxisomeproliferator activated receptor a (PPARa) activation. We previously foundliver lipid overaccumulation and no response to leptin-induced lipid catabolicactions in foetuses from rats fed with an overload of fat (SFD).Objective: to analyse whether foetuses and offspring from the SFD grouprespond to the lipid catabolic effects of the PPARa activator clofibrate.Methods: Female rats were fed with standard (controls) or saturated fatdiet (28% fat) since they were 6 week-old (SFD rats). After 8 weeks, theywere mated with control males. Control and SFD rats were euthanized atgestational day 21 or allowed to deliver and their offspring euthanized at140 days of age. Offspring and foetal livers were cultured (3h) (n¼6) withor without clofibrate (0.1mM). Lipid levels (triglycerides (TG), phospholipids(PL), free fatty acids (FA) and cholesteryl esters (CE)) were assessedby TLC. ACO and CPT1 expression was analysed by PCR.Results: In livers from control foetuses, clofibrate decreased lipid levels(females: TG, FA, and EC 25%, males: PL and FA 30%, P