Mol. Hum. Reprod. Advance Access published online on July 16, 2004
Molecular Human Reproduction, doi:10.1093/molehr/gah090
© 2004 by Oxford University Press
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1 Laboratory of Reproduction and Metabolism, CEFYBO-CONICET, Serrano 669, C1414DEM Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: elidate{at}fibertel.com.ar.
Diabetes induces alterations which condition placental remodelling. The levels of nitric oxide (NO) (a modulator of placental invasiveness, differentiation and proliferation) were higher in term placental explants from diabetic patients when compared to controls. Peroxisome proliferator-activated receptor
Revised June 19, 2004
Accepted June 25, 2004
Article
Influence of peroxisome proliferator-activated receptor
activation by its endogenous ligand 15-deoxy 
12,14 prostaglandin J2 on nitric oxide production in term placental tissues from diabetic women
2 Obstetrics, Carlos G.Durand Hospital, Buenos Aires, C1414DEM, Argentina
3 Nutrition Departments, Carlos G.Durand Hospital, Buenos Aires C1414DEM, Argentina
Abstract 
(PPAR) activation by its endogenous ligand 15-deoxy 
12,14prostaglandin J2 (15dPGJ2), is a differentiating factor of adipocytes and other cell types, such as trophoblasts. 15dPGJ2 is also able to down-regulate NO production in different cell types. Our study evaluated the levels of 15dPGJ2 and PPAR and the influence of PPAR activation by 15dPGJ2 on the production of NO, in term placental tissues from control, pre-gestational and gestational diabetic patients. Our results showed that 15dPGJ2 was present in human term placenta, and that its levels were diminished in gestational (P<0.05) and pre-gestational (P<0.002) diabetic women when compared to controls. Exogenous 15dPGJ2 addition (2 x 10-6 mol/l) down-regulated NO production in placenta from control (P<0.001) and pre-gestational diabetic (P<0.01) patients, but failed to do so in gestational diabetic women, whose placental PPAR expression was diminished in comparison to controls (P<0.001). As the exogenous activation of PPAR prevented NO overproduction in placenta from pre-gestational diabetic women, it may have the potential to improve fetal outcome in this pathology.; 15dPGJ2.
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