non-alcoholic fatty liver disease Archives - Revista Brasileira de Ginecologia e Obstetrícia
, , , , Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2024;46:e-rbgo81
, , , , To verify the prevalence and factors associated with Non-Alcoholic Fatty Liver Disease (NAFLD) among women with Polycystic Ovary Syndrome (PCOS).
A cross-sectional study was conducted with 53 patients with PCOS. The diagnosis of PCOS followed the Rotterdam criteria. The diagnosis of NAFLD was made through US showing hepatic steatosis, excluding significant alcohol consumption and chronic liver disease. The following variables were compared between the groups of women with and without NAFLD: age, race, anthropometric data, blood pressure levels, liver enzymes, glycemic and lipid profiles, total testosterone, presence of hirsutism, and metabolic syndrome (MS). Variables were compared between the groups using T-test, Mann-Whitney, and Chi-square tests.
Among 53 patients with PCOS, 50.9% had NAFLD. The NAFLD group had higher weight (p=0.003), BMI (p=0.001), waist circumference (p≤0.001), fasting glucose (p=0.021), HbA1C% (p=0.028), triglycerides (p=0.023), AST (p=0.004), ALT (p=0.001), higher prevalence of MS (p=0.004), and lower levels of HDL cholesterol (p=0.043). The other variables did not differ between the groups. Both groups were predominantly of caucasian race, and there was no significant difference in age.
The prevalence of NAFLD among patients with PCOS was 50.9%. Metabolic and hepatic enzyme abnormalities were more prevalent in this group compared to the group without the disease. Obesity tripled the prevalence of NAFLD.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2024;46:e-rbgo81
, , , , To verify the prevalence and factors associated with Non-Alcoholic Fatty Liver Disease (NAFLD) among women with Polycystic Ovary Syndrome (PCOS).
A cross-sectional study was conducted with 53 patients with PCOS. The diagnosis of PCOS followed the Rotterdam criteria. The diagnosis of NAFLD was made through US showing hepatic steatosis, excluding significant alcohol consumption and chronic liver disease. The following variables were compared between the groups of women with and without NAFLD: age, race, anthropometric data, blood pressure levels, liver enzymes, glycemic and lipid profiles, total testosterone, presence of hirsutism, and metabolic syndrome (MS). Variables were compared between the groups using T-test, Mann-Whitney, and Chi-square tests.
Among 53 patients with PCOS, 50.9% had NAFLD. The NAFLD group had higher weight (p=0.003), BMI (p=0.001), waist circumference (p≤0.001), fasting glucose (p=0.021), HbA1C% (p=0.028), triglycerides (p=0.023), AST (p=0.004), ALT (p=0.001), higher prevalence of MS (p=0.004), and lower levels of HDL cholesterol (p=0.043). The other variables did not differ between the groups. Both groups were predominantly of caucasian race, and there was no significant difference in age.
The prevalence of NAFLD among patients with PCOS was 50.9%. Metabolic and hepatic enzyme abnormalities were more prevalent in this group compared to the group without the disease. Obesity tripled the prevalence of NAFLD.
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.
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.
