Lipid metabolism in the embryos of diabetic rats during early organogenesis: modulatory effect of prostaglandin E2
Debora Sinner A D , J. Matías Caviglia B D , Alicia Jawerbaum A C , R. Ariel Igal B and Elida Gonzalez AA Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Serrano 669, (1414) Buenos Aires, Argentina.
B Instituto de Investigaciones Bioquímicas de La Plata, Facultad de Ciencias Médicas, CONICET and Universidad Nacional de La Plata, Calles 60 y 120, (1900) La Plata, Argentina.
C To whom correspondence should be addressed. email: a.jawerbaum@abaconet.com.ar
D *D. Sinner and J. M. Caviglia equally contributed to this work
Reproduction, Fertility and Development 15(1) 75-80 https://doi.org/10.1071/RD02068
Submitted: 19 August 2002 Accepted: 7 February 2003 Published: 7 February 2003
Abstract
The purpose of this work was to evaluate de novo lipid biosynthesis and the lipid profile, and to study the effect of prostaglandin E2 (PGE2; prostaglandin has previously been found to be involved in diabetes embryopathy) on lipid metabolism in embryos from control and streptozotocin-induced diabetic rats during organogenesis. Increased levels of triacylglycerols were found in embryos of diabetic rats compared with controls, whereas no differences were detected in the levels of cholesterol, cholesterylester, phosphatidylcholine and phosphatidylethanolamine. When the de novo synthesis of lipids in the embryo was studied using [14C]acetate as a tracer, a diminished rate of incorporation of [14C]acetate into the evaluated lipid classes was detected in the diabetic embryo compared with controls. Addition of PGE2 did not modify the incorporation of [14C]acetate into any of the lipid species of control embryos, but enhanced the incorporation of [14C]acetate into triacylglycerol, cholesterylesters, phosphatidylcholine and phosphatidylethanolamine of embryos from diabetic rats. The study’s results show alterations in both synthesis and concentrations of lipids in the embryos of diabetic rats. Interestingly, the results demonstrate that the addition of PGE2, a prostaglandin that reverses the embryonic morphological abnormalities induced by diabetes, prevents disturbances in embryo lipid synthesis caused by diabetes.
Extra keywords: diabetes in pregnancy
Acknowledgments
This work has been supported by grants from from Ministerio de Salud de la Nación Argentina, ‘Ramón Carrillo-Arturo Oñativia’ (A.J.), by Agencia Nacional de Promoción Científica y Tecnológica PICT98 05-03375 (E.G.) and PICT98 06-03823 (R.A.I.) and by the National Institutes of Health (NIH, USA) TW00891 (R.A.I.). Debora Sinner is a recipient of a PROGRESAR program fellowship, ICMER, Chile. J. Matías Caviglia is a Doctoral Fellow from CONICET, Argentina. Alicia Jawerbaum, R. Ariel Igal and Elida Gonzalez are investigators from CONICET, Argentina.
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