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  • Title: Study of changes in antioxidant enzymes status in diabetic post menopausal group of women suffering from cardiovascular complications.
    Author: Kumawat M, Sharma TK, Singh N, Ghalaut VS, Vardey SK, Sinha M, Kaushik GG.
    Journal: Clin Lab; 2012; 58(3-4):203-7. PubMed ID: 22582492.
    Abstract:
    BACKGROUND: In type 2 diabetic patients, persistence of hyperglycemia has been reported as a cause of increased production of oxygen free radicals (FR), which leads to oxidative stress (OS) and becomes the main factor for predisposition to the cardiovascular complications in diabetes. Diabetic postmenopausal women are prone to cardiovascular disease due to reduced production of estrogen which is a potent antioxidant and prevents oxidative stress (OS) in body. The study is being aimed to find out the status of antioxidant enzymes (AOEs) and malondialdehyde (MDA) in post-menopausal diabetic women. METHODS: The study was conducted with a total of 70 cases, which included 35 Type 2 diabetic post-menopausal females (45 - 60 years) with diabetic CVD complication as the study group and 35 age matched type 2 diabetic postmenopausal females without CVD complication. RESULTS: All diabetic post menopausal females with CVD had significantly higher levels of fasting plasma glucose (FPG), postprandial plasma glucose (PPPG), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), catalase (CAT), and malondialdehyde (MDA) and significantly lower levels of HDL-C, reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), and superoxide dismutase (SOD) as compared to the levels of control subjects. CONCLUSIONS: During menopause, reduced production of estrogen causes hypertriglyceridemia, hypercholesterolemia, and hyperlipoproteinemia whose oxidation causes the accumulation of FR in the cell, which precipitates OS. Also, type 2 diabetic subjects with CVD poor glycemic control and impaired AOEs result in increased oxidative injury by failure of protective mechanisms, which further leads to oxidative stress.
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