Effects of PPAR activation in the placenta and the fetus: implications in maternal diabetes.

JAWERBAUM ALICIA; CAPOBIANCO EVANGELINA

PLACENTA

W B SAUNDERS CO LTD

Año: 2011 vol. 32 p. 212 - 217

0143-4004

Peroxisome proliferator activated receptors (PPARalfa, PPARgamma and PPARdelta) are ligand activated transcription factors that regulate metabolic, anti-inflammatory and developmental processes. The maternal and fetal metabolic impairments, the intrauterine pro-inflamatory environment and the developmental defects induced by maternal diabetes make PPARs an interesting focus of investigation. Therefore, research has been conducted in experimental models of diabetes throughout gestation. During embryo organogenesis, impaired PPARdelta signalling pathways are related to the induction of congenital malformations. In fetuses from diabetic rats, lipid metabolism, lipid peroxidation and several pro-inflammatory markers are regulated by the activation of the three PPAR isotypes. In the placenta from diabetic animals, activation of different PPAR isotypes regulates lipid metabolism and anti-inflammatory pathways, whereas in term placentas from diabetic patients, PPARs regulates nitric oxide overproduction. Decreased PPARgamma and PPARalpha expression are found in the placenta from diabetic animals and diabetic patients. Besides, deficiency in polyunsaturated fatty acids (PUFAs) and impaired formation of arachidonic acid derivatives that activate PPARs is characteristic in diabetic intrauterine tissues. PPARs can be activated by both natural and pharmacological activators. Intrauterine activation of PPARs can be achieved by the administration of maternal diets enriched in PUFAs. This review summarizes recent advances highlighting the possible beneficial role of PPARs activation in embryo and feto-placental development in maternal diabetes.