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Mol. Hum. Reprod. Advance Access originally published online on December 5, 2006
Molecular Human Reproduction 2007 13(2):103-110; doi:10.1093/molehr/gal104
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© The Author 2006. 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

PPAR{delta} and its activator PGI2 are reduced in diabetic embryopathy: involvement of PPAR{delta} activation in lipid metabolic and signalling pathways in rat embryo early organogenesis

R. Higa, E. González, M.C. Pustovrh, V. White, E. Capobianco, N. Martínez and A. Jawerbaum1

Laboratory of Reproduction and Metabolism, CEFYBO-CONICET, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina

1 To whom correspondence should be addressed at: Laboratory of Reproduction and Metabolism, CEFYBO-CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, Buenos Aires (C1121ABG), Argentina. E-mail: a.jawerbaum{at}abaconet.com.ar


  Abstract

Maternal diabetes significantly increases the risk of congenital malformations, and the mechanisms involved are not yet clarified. This study was designed to address peroxisome proliferator-activated receptor {delta} (PPAR{delta}) involvement in diabetic embryopathy. We investigated the concentrations of PPAR{delta} and its endogenous agonist prostaglandin (PG)I2, as well as the effect of PPAR{delta} activation on lipid metabolism and PGE2 concentrations in embryos from control and streptozotocin-induced diabetic rats during early organogenesis. Embryos from diabetic rats showed decreased concentrations of PPAR{delta} and its endogenous agonist PGI2 when compared with controls. In embryos from control rats, the addition of the PPAR{delta} activators (cPGI2 and PGA1) increased embryonic phospholipid levels and de novo phospholipid synthesis studied using 14C-acetate as a tracer. PGE2 formed from arachidonate released from phospholipid stores was also up-regulated by PPAR{delta} activators. In embryos from diabetic rats, reduced phospholipid synthesis and PGE2 content were observed, and clearly up-regulated by cPGI2 additions to values similar to those found in control embryos. These data suggest that PPAR{delta} may play an important role in lipid metabolic and signalling pathways during embryo organogenesis, developmental pathways that are altered in embryos from diabetic rats, possibly as a result of a reduction in levels of PPAR{delta} and its endogenous activator PGI2.

Key words: diabetes in pregnancy/lipid mediators/embryo development/PPARs/prostaglandins


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