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You searched for:"Emy Luiza Ishii-Iwamoto"
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Revista Brasileira de Ginecologia e Obstetrícia. 2018;40(5):251-259
The aim of this work was to evaluate the changes caused by estrogen deficiency in lipid metabolism.
This study encompassed direct measurements of plasma biochemical analyses, liver lipid contents, and assessments of the mitochondrial β-oxidation capacity as well as an evaluation of the liver redox status in an animal model of estrogen deficiency.
When compared with control mice, the livers of ovariectomized (OVX) mice presented considerable accretions in their lipid contents, which were accompanied by increased levels of lipid peroxidation in liver homogenates andmitochondria from OVX groups and decreased reduced glutathione (GSH) contents. In isolated mitochondria, estrogen deficiency inhibited mitochondrial β-oxidation of fatty acids irrespective of their chain length. The liver mitochondrial and peroxisomal H2O2 generations in OVX mice were increased. Additionally, the activities of all antioxidant enzymes assessed were decreased.
These data provide one potential explanation for the increased susceptibility to metabolic diseases observed after menopause.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2018;40(5):251-259
The aim of this work was to evaluate the changes caused by estrogen deficiency in lipid metabolism.
This study encompassed direct measurements of plasma biochemical analyses, liver lipid contents, and assessments of the mitochondrial β-oxidation capacity as well as an evaluation of the liver redox status in an animal model of estrogen deficiency.
When compared with control mice, the livers of ovariectomized (OVX) mice presented considerable accretions in their lipid contents, which were accompanied by increased levels of lipid peroxidation in liver homogenates andmitochondria from OVX groups and decreased reduced glutathione (GSH) contents. In isolated mitochondria, estrogen deficiency inhibited mitochondrial β-oxidation of fatty acids irrespective of their chain length. The liver mitochondrial and peroxisomal H2O2 generations in OVX mice were increased. Additionally, the activities of all antioxidant enzymes assessed were decreased.
These data provide one potential explanation for the increased susceptibility to metabolic diseases observed after menopause.
