15-DEOXY D12,14PROSTAGLANDIN J2 MODULATES THE LIPID SYNTHESIS IN TERM PLACENTAS FROM HEALTHY AND GESTATIONAL DIABETIC PATIENTS.

CAPOBIANCO E, JAWERBAUM A, WHITE V, PUSTOVRH C, MARTÍNEZ N, HIGA R, GONZÁLEZ E.

Santiago de Chile, Chile

Simposio; 2nd Latin-American symposium on maternal-fetal interaction and placenta: Research & Clinical studies; 2005

Sociedad Latino-Americana de Interacción Materno Fetal y Placenta

Diabetes mellitus affects placental lipid metabolism. 15-deoxy D12,14prostaglandinJ2 (15dPGJ2) is a high affinity endogenous ligand for the peroxisome proliferator-activated receptor g (PPARgamma) which regulates the transcription of genes involved in lipid and glucose homeostasis. The aim of this study was to determine whether 15dPGJ2 is able to regulate lipid metabolism in term placentas from healthy patients (CP) and gestational diabetic patients (GDP). Methods: Placental tissues from CP and GDP were obtained at term. Villous samples were taken and incubated for 3 h either with or without 15dPGJ2 (2x10-6 mol/l) for further evaluation of both lipid mass (by TLC and image analysis) and the de novo lipid synthesis (by determining the incorporation of 14C-acetate to lipids). Results: The synthesis of cholesteryl ester (CE) (p<0.05), triglycerides (TG) (p<0.01), free fatty acids (FFA) (p<0.05) and phospholipids (PL) (p<0.05) was decreased in placentas from GDP compared with CP. No differences were found in lipid mass from both groups. The addition of 15dPGJ2 decreased the synthesis of TG (p<0.05) and cholesterol (CHO) (p<0.05) in placentas from CP and GDP. In GDP the synthesis of CE (p<0.01), and FFA (p<0.001) was also reduced. 15dPGJ2 did not modify the levels of the lipids evaluated in both groups. Conclusions: Gestational diabetes reduces the ability of placental de novo lipid synthesis, a pathway that serves to the accretion of placental lipids from carbon moieties, and that is negatively regulated in both CP and GDP by the PPARgamma agonist 15dPGJ2.