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Decreased mitochondrial fatty acid oxidation in placentas from women with preeclampsia
J L Bartha1, F Visiedo, A Fernández-Deudero
1Division of Maternal and Fetal Medicine, Department of Obstetrics and Gynecology, University Hospital Puerta del Mar, Cádiz, Spain. joseluis.bartha@uca.es
Preeclampsia is a leading cause of maternal and fetal morbidity and mortality in high and low-income countries. The aetiology of preeclampsia is multifactorial and remains obscure. Some evidences suggest that altered placental fatty acid oxidation might play a role in the pathogenesis of preeclampsia. To reveal if placental fatty acid oxidation is reduced in preeclampsia, we evaluate the expression levels of enzymes of mitochondrial fatty acid oxidation using quantitative Real-time PCR and the fatty acid oxidation rate in placental explants. We found that long-chain 3-hydroxyacyl-CoA dehydrogenase levels and fatty acid oxidation capacity were significantly reduced in placentas from women with preeclampsia.
Preeclampsia is a leading cause of maternal and fetal morbidity and mortality in high and low-income countries. The aetiology of preeclampsia is multifactorial and remains obscure. Some evidences suggest that altered placental fatty acid oxidation might play a role in the pathogenesis of preeclampsia. To reveal if placental fatty acid oxidation is reduced in preeclampsia, we evaluate the expression levels of enzymes of mitochondrial fatty acid oxidation using quantitative Real-time PCR and the fatty acid oxidation rate in placental explants. We found that long-chain 3-hydroxyacyl-CoA dehydrogenase levels and fatty acid oxidation capacity were significantly reduced in placentas from women with preeclampsia.

