Role of impaired lipid metabolism in diabetes and pregnancy complications

JAWERBAUM A

Pucón, Chile

Congreso; XXII Congreso de la Asociación Latino-Americana de Ciencias Fisiológicas (ALACF), II Congreso Iberoameriano de Ciencias Fisiológicas. XXXIII Reunión de la Sociedad Chilena de Ciencias Fisiológicas (SCHCF); 2009

Sociedad de Biología de Chile

The altered lipid metabolism induced by maternal diabetes complicates embryonic and feto-placental development. The main feature is the excess of lipids present in the mother and all intrauterine tissues. Fetal lipid accretion is related to the increased placental transport of glucose and lipids, and to alterations in several placental lipid metabolic pathways. These impairments lead to an excess of lipids and, due to the intrauterine pro-inflammatory environment, to an increase in lipid peroxidation during development. The other important feature of the impaired lipid metabolism that arises in diabetic pregnancies is the deficiency in essential fatty acids (EFAs), which will profoundly affect embryo development. EFAs deficiency is clearly involved in maternal diabetes-induced congenital malformations. In addition, EFAs have important functions as signaling molecules in feto-placental development and metabolism. Indeed, they are ligands of the nuclear receptors PPARs, and substrates for the synthesis of prostaglandins that are also ligands of these nuclear receptors. Interestingly, PPARs have been recently identified as important regulators of feto-placental lipid homeostasis. Dietary activation of PPARs in maternal diabetes is able to prevent lipid accretion and reduce lipid peroxidation in the fetus. In conclusion, maternal diabetes-induced lipid excess and EFAs deficiency have adverse consequences during the embryonic and feto-placental development. Modulation of the quality/quantity of dietary lipids may be helpful to regulate feto-placental lipid metabolism, pro-inflammation and development in diabetic gestations.