PPAR activation as a regulator of lipid metabolism, nitric oxide production and lipid peroxidation in the placenta from type 2 diabetic patients.

CAPOBIANCO E, MARTÍNEZ N, FORNES D, HIGA R, ; DI MARCO I, BASUALDO MN; FAINGOLD MC; JAWERBAUM

MOLECULAR AND CELLULAR ENDOCRINOLOGY.

ELSEVIER IRELAND LTD

Lugar: Amsterdam; Año: 2013 vol. 377 p. 7 - 15

0303-7207

Peroxisome Proliferator Activated Receptors (PPARs) are ligand activated transcription factors with crucial functions in lipid homeostasis, anti-inflammatory processes and placental development. Maternal diabetes induces a pro-inflammatory environment and alters placental development. We investigated whether PPARs regulate lipid metabolism and nitric oxide (NO) production in placental explants from healthy and type 2 diabetic (DM2) patients. We found decreased PPARalpha and PPARgamma concentrations, no changes in PPARdelta concentrations, and increased lipids, lipoperoxides and NO production in placentas from DM2 patients. PPARalfa agonists reduced placental concentrations of triglycerides and both PPARalfa and PPARdelta agonists reduced concentrations of phospholipids, cholesteryl esters and cholesterol. PPARgamma agonists increased lipid concentrations in placentas from DM2 patients and more markedly in placentas from healthy patients. Endogenous ligands for the three PPAR isotypes reduced NO production and lipoperoxidation in placentas from DM2 patients. We conclude that PPARs play a role in placental NO and lipid homeostasis and can regulate NO production, lipid concentrations and lipoperoxidation in placentas from DM2 patients.