CEFYBO 02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
artículos
Título:
Safflower-oil and olive-oil dietary treatments rescues aberrant embryonic arachidonic acid and nitric oxide metabolism, and prevents diabetic embryopathy in rats
Autor/es:
HIGA R; WHITE V; MARTÍNEZ N; KURTZ M; CAPOBIANCO E; JAWERBAUM A.
Revista:
MOLECULAR HUMAN REPRODUCTION.
Editorial:
Oxford University Press
Referencias:
Lugar: Oxford; Año: 2010 vol. 16 p. 286 - 295
ISSN:
1360-9947
Resumen:
Aberrant arachidonic acid and nitric oxide (NO) metabolic pathways are involved in diabetic embryopathy. Previous works have found diminished concentrations of PGE2 and PGI2 in embryos from diabetic rats, and that PGI2 is capable of increasing embryonic PGE2 concentrations through the activation of the nuclear receptor PPARd. PPARd activators are lipid molecules such as oleic and linoleic acids, present in high concentrations in olive and safflower oils respectively. The aim of this study was to analyze the capability of dietary supplementation with either 6% olive or 6% safflower oils to regulate PGE2, PGI2 and NO concentrations in embryos and decidua from control and diabetic rats during early organogenesis. Diabetes was induced by a single injection of streptozotocin (55mg/kg) one week before mating. Animals were fed with the oil-supplemented diets from days 0.5 to 10.5 of gestation. PGI2 and PGE2 were measured by EIA and NO through the evaluation of its stable metabolites nitrates/nitrites in 10.5-day embryos and decidua. We found that the olive- and safflower-oil supplemented treatments highly reduced resorption and malformation rates in diabetic animals, and that they were able to prevent maternal diabetes-induced alterations in embryonic and decidual PGI2 and PGE2 concentrations. Moreover, these dietary treatments prevented NO overproduction in embryos and decidua from diabetic rats. These data indicate that in maternal diabetes both the embryo and the deciduum benefit from the olive-oil and safflower-oil supplementation probably through mechanisms that involve the rescue of aberrant prostaglandin and NO generation and that prevent developmental damage during early organogenesis.
