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

FLORENCIA HEINECKE, MARTINA RADICE, M.BELÉN MAZZUCCO, ALICIA JAWERBAUM, VERÓNICA WHITE

Puerto Varas

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

Leptin induces liver lipid catabolism, increasing acetyl CoA oxidase (ACO) and carnitin palmitoyl transferase-1 (CPT1) expression, through peroxisome proliferator activated receptor alpha (PPARalpha) 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 analyze whether fetuses and offspring from the SFD group respond to the lipid catabolic effects of the PPARalpha 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) with or without clofibrate (0.1 microM). Lipid levels (Triglycerides (TG), phospholipids (PL), free fatty acids (FA) and cholesteryl esters (CE)) by TLC, and ACO and CPT1 expression by PCR were assessed. Results: In livers from control fetuses, clofibrate decreased lipid levels (Females TG, FA and EC 25%, Males: PL and FA: 30%, p