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

CAPOBIANCO E,; MARTINEZ N,; FORNES D,; HIGA R,; DI MARCO I,; BASUALDO MN; FAINGOLD C,; JAWERBAUM A,

MOLECULAR AND CELLULAR ENDOCRINOLOGY.

ELSEVIER IRELAND LTD

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

0303-7207

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