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Mol. Hum. Reprod. Advance Access originally published online on July 11, 2008
Molecular Human Reproduction 2008 14(8):491-499; doi:10.1093/molehr/gan039
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Effects of natural ligands of PPAR{gamma} on lipid metabolism in placental tissues from healthy and diabetic rats

Evangelina Capobianco, Verónica White, Romina Higa, Nora Martínez and Alicia Jawerbaum1

Laboratory of Reproduction and Metabolism, CEFYBO-CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, Buenos Aires C1121ABG, Argentina

1 Correspondence address. E-mail: a.jawerbaum{at}abaconet.com.ar

Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) is a ligand-dependent nuclear receptor that plays an important role in placental development and function metabolism in diabetic and control rats after midpregnancy, as well as the concentrations of the PPAR{gamma} endogenous agonist 15deoxy{Delta}12,14Prostaglandin J2 (15dPGJ2). In vitro experiments showed that 15dPGJ2 did not regulate placental concentrations of triglycerides, cholesteryl esters, phospholipids and free fatty acids, but decreased the de novo synthesis of these lipid species. PPAR agonists were administered in vivo through dietary supplementation with either 6% olive oil or 6% safflower oil. These treatments led to increases in placental lipid mass in control tissues and more markedly in diabetic tissues. In addition, they led to reductions in the de novo lipid synthesis both in control and in diabetic placental tissues. In the placenta from diabetic rats fed with the standard diet, 15dPGJ2 concentrations were greatly reduced. Both dietary supplementations increased the concentrations of 15dPGJ2 in placentas from control and diabetic rats. These data indicate that, in the placenta, PPAR{gamma} natural ligands regulate the concentration of their own endogenous ligands. In addition, they increase the placental capacity to accumulate maternal-derived lipids, and reduce the de novo lipid synthesis, thus regulating metabolic pathways that are altered in the placenta from diabetic rats and involved in the lipid transfer to the developing fetus.

Key words: diabetes in pregnancy/lipids/placenta/PPARs/prostaglandins

Submitted on February 28, 2008; resubmitted on June 25, 2008; accepted on June 27, 2008.


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