Peroxisome proliferators activated receptors (PPARs) involvement in lipid homeostasis in fetuses from control and diabetic rats.

KURTZ MELISA; WHITE VERÓNICA; CAPOBIANCO EVANGELINA; JAWERBAUM ALICIA

Concepción, Chile

Congreso; 8TH International Post graduate Workshop 2º ICPD International course of Pregnancy diseases; 2009

International Post graduate Workshop 2º ICPD

Previous works have shown the capability of PPARalpha and PPARgamma agonists to modulate lipid metabolism in placentas from control and diabetic rats. However, the functions of PPARdelta, a PPAR isoform essential in placental development, are less known. We analyzed whether the activation of PPARdelta modulates lipid metabolism in placentas from control (C) and diabetic (D) rats. Diabetes was induced by neonatal streptozotocin administration. Placentas were explanted on day 13.5 of gestation and incubated with and without addition of carbaprostacyclin, cPGI2 (1µM), a stable analogous of PGI2 capable of activating PPARdelta. Lipids levels were measured using TLC and densitometry, the de novo lipid synthesis using 14 C acetate as a tracer, and lipid catabolism by evaluating glycerol release. PGI2 was measured by EIA. Triglycerides and cholesteryl esters concentrations were increased in D placentas when compared to C (p<0,01), and the addition of cPGI2 diminished the levels of phospholipids (p<0,05), cholesterol (p<0,001) and free fatty acid (p<0,05) in D placentas. Lipid catabolism was enhanced in D placentas compared to C (p<0,01), cPGI2 increased this parameter in C and D tissue. De novo lipid synthesis was reduced in D placentas when compared to C (p<0,01), and cPGI2 further reduced this parameter (p<0,05). PGI2 levels were diminished in D placentas when compared to C (p<0,02). In conclusion, this work supports the capability of cPGI2 to regulate placental lipid metabolism. The observed effects were more evident in the diabetic placenta, which present alterations not only in lipid metabolism parameters but also in PGI2 concentrations.