PPARalpha agonists modulate lipid and nitridergic metabolism in term placenta from control and diabetic rats.

MARTÍNEZ NORA; CAPOBIANCO EVANGELINA; FERNÁNDEZ DO PORTO DARÍO; JAWERBAUM ALICIA; GONZÁLEZ ELIDA

Los Cocos, Córdoba

Simposio; III Latin American Symposium on Maternal Fetal Interaction and Placenta: Basic & Clinical Research.; 2007

Asociación Latinoamericana de estudio de la Interacción Materno Fetal y la placenta

Diabetes alters placental lipid and nitric oxide (NO) metabolism. PPARa is a nuclear receptor involved in lipid homeostasis. We aimed to evaluate whether PPARa agonists regulate lipid levels, NO production and lipid peroxidation in the placenta from control (C) and diabetic (D) rats at term. Methods: Diabetes was induced by streptozotocin administration to rat neonates (90 mg/kg). Placental explants obtained at term were cultured for 3h either with or without the PPARa agonists clofibrate (20 µM) and LTB4 (0.1 mM) for further analysis of 1) Lipid levels by TLC and densitometry, 2) NO production by measurement of nitrates/nitrites and 3) Lipid peroxidation by determination of thiobarbituric acid reactive substances (TBARs). Results: Both LTB4 and clofibrate reduced placental concentrations of cholesterol (p<0.05), triglycerides (p<0.01) and cholesteryl esters (P<0.05) when compared to controls without additions. These PPARa agonists diminished NO levels (p<0.05) in both C and D placenta. PPARa activation did not modify TBARs levels in C rats. Lipid peroxidation was enhanced in D placenta when compared to C (p<0.01), and the addition of the PPARa agonist clofibrate reduced TBARs levels in D placenta (p<0.01). Conclusions: Our results provide evidence of the role of PPARa in the regulation of lipid levels, NO production and lipid peroxidation in rat term placenta. Therefore, PPARa activation may help to prevent placental alterations induced by maternal diabetes.