| dc.description.abstract |
The purpose of this work was to evaluate de novo lipid biosynthesis and the lipid profile, and to study the effect of prostaglandin E<emph type="8">2 (PGE<emph type="8">2; 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 [<emph type="7">14C]acetate as a tracer, a diminished rate of incorporation of [<emph type="7">14C]acetate into the evaluated lipid classes was detected in the diabetic embryo compared with controls. Addition of PGE<emph type="8">2 did not modify the incorporation of [<emph type="7">14C]acetate into any of the lipid species of control embryos, but enhanced the incorporation of [<emph type="7">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 PGE<emph type="8">2, a prostaglandin that reverses the embryonic morphological abnormalities induced by diabetes, prevents disturbances in embryo lipid synthesis caused by diabetes. |
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