PPARδ and its activator PGI2 are reduced in diabetic embryopathy: involvement of PPARδ activation in lipid metabolic and signalling pathways in rat embryo early organogenesis | Zendy

Romina Higa | Zendy; Ezequiel González | Zendy; María Carolina Pustovrh | Zendy; Verónica White | Zendy; Evangelina Capobianco | Zendy; Nora Martínez | Zendy; Alicia Jawerbaum | Zendy

Open Access

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

Author(s) -

Romina Higa,

Ezequiel González,

María Carolina Pustovrh,

Verónica White,

Evangelina Capobianco,

Nora Martínez,

Alicia Jawerbaum

Publication year - 2006

Publication title -

molecular human reproduction

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.143

H-Index - 122

eISSN - 1460-2407

pISSN - 1360-9947

DOI - 10.1093/molehr/gal104

Subject(s) - biology , peroxisome proliferator activated receptor , activator (genetics) , embryo , signalling pathways , organogenesis , endocrinology , signal transduction , medicine , lipid metabolism , signalling , peroxisome , lipid signaling , hedgehog signaling pathway , microbiology and biotechnology , receptor , biochemistry , gene

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 (PPARdelta) involvement in diabetic embryopathy. We investigated the concentrations of PPARdelta and its endogenous agonist prostaglandin (PG)I(2), as well as the effect of PPARdelta activation on lipid metabolism and PGE(2) concentrations in embryos from control and streptozotocin-induced diabetic rats during early organogenesis. Embryos from diabetic rats showed decreased concentrations of PPARdelta and its endogenous agonist PGI(2) when compared with controls. In embryos from control rats, the addition of the PPARdelta activators (cPGI(2) and PGA(1)) increased embryonic phospholipid levels and de novo phospholipid synthesis studied using (14)C-acetate as a tracer. PGE(2) formed from arachidonate released from phospholipid stores was also up-regulated by PPARdelta activators. In embryos from diabetic rats, reduced phospholipid synthesis and PGE(2) content were observed, and clearly up-regulated by cPGI(2) additions to values similar to those found in control embryos. These data suggest that PPARdelta 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 PPARdelta and its endogenous activator PGI(2).

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