Effects of maternal diabetes or in vitro hyperglycemia on uptake of palmitic and arachidonic acid by rat embryos.

Altered transfer of nutrients from mother to conceptus may be involved in the pathogenesis of the developmental disturbances in offspring of diabetic mothers. In our study, the embryonic uptake of a saturated (palmitic acid) and a nonsaturated (arachidonic acid) fatty acid was evaluated in a normal and a diabetes-like environment under in vivo and in vitro conditions that yield growth retardation and somatic malformations in the embryos. The palmitic acid uptake in embryos from diabetic rats and in embryos cultured in vitro in 30 mmol/L D-glucose did not differ from the respective controls. Only embryos cultured in the highest D-glucose concentration (60 mmol/L) showed slightly increased uptake, which suggests that alterations in palmitic acid transfer have no role in the processes of embryonic maldevelopment in diabetic pregnancy. In contrast, the results showed that a diabetes-like environment both in vivo and in vitro causes increased embryonic uptake of arachidonic acid. Consequently, if the teratogenic mechanisms of diabetic pregnancy involve decreased embryonic levels of arachidonic acid, as has been suggested, this would not be the effect of a decreased uptake per se, but rather of an altered intracellular metabolism or decreased extracellular availability of this fatty acid.