Background:Oxidative stress has been considered to be a pathogenic factor of diabetic complications including nephropathy. There are many controversies and limited studies regarding the antioxidant enzymes in diabetic nephropathy.Aim:This study was to evaluate the levels of antioxidant enzymes and lipid peroxidation in Type-2 Diabetes Mellitus (DM) patients with and without nephropathy.Materials and Methods:The study included 90 age and sex matched subjects. Blood samples of all subjects were analyzed for all biochemical and oxidative stress parameters.Results:The malondialdehyde (MDA) levels and catalase (CAT) activity were significantly increased and reduced glutathione (GSH) levels and activities of glutathione peroxidase (GPx) and glutathione reductase (GR) were significantly decreased in Type-2 DM with and without nephropathy as compared to controls and also in Type-2 DM with nephropathy as compared to Type-2 DM without nephropathy. There were an excellent positive correlation of glycohemoglobin (HbA1c) with MDA and a good negative correlation of GPx with GSH in controls. There were positive correlations of GR, CAT, and superoxide dismutase (SOD) with MDA in Type-2 diabetes patients with nephropathy.Conclusions:Intensity of oxidative stress in Type-2 diabetic patients with nephropathy is greater when compared with Type-2 diabetic patients without nephropathy as compared to the controls.
In diabetic patients, persistence of hyperglycemia has been reported as a cause of increased production of oxygen free radicals. Hyperglycemia could induce oxidative stress and become the main factor for predisposing the complications in diabetes. The study is being aimed to find out the status of lipid peroxidation product i.e. malondialdehyde (MDA) and antioxidant enzymes (AOEs) such as glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) which might be helpful in risk assessment of various complications of diabetes mellitus. The study included 300 subjects (50-70yrs) out of which 150 patients were non insulin dependent diabetes mellitus (NIDDM) with micro vascular complications and 150 age matched healthy controls. The status of fasting blood sugar (FBS), reduced glutathione (GSH), GPx, GR, CAT, SOD and MDA were determined. Our results showed significant increase (p< 0.001) in FBS, CAT and MDA while GSH, GPx, GR and SOD were found decreased significantly (p< 0.001). The data suggest that alteration in antioxidant status and MDA may help to predict the risk of various micro vascular complications of diabetes mellitus.
SummaryThe transcriptional activator Zap1p maintains zinc homeostasis in Saccharomyces cerevisiae. In this study, we examined the role of Zap1p in triacylglycerol (TAG) metabolism. The expression of ETR1 is reduced in zap1D. The altered expression of ETR1 results in reduced mitochondrial fatty acid biosynthesis and reduction in lipoic acid content in zap1D. The transcription factor Zap1 positively regulates ETR1 expression. Deletion of ETR1 also causes the accumulation of TAG, and the introduction of ETR1 in zap1D strain rescues the TAG level. These results demonstrated that the compromised mitochondrial fatty acid biosynthesis causes a reduction in lipoic acid and loss of mitochondrial function in zap1D. Functional mitochondria are required for the ATP production and defect in mitochondria slow down the process which may channeled carbon towards lipid biosynthesis and stored in the form of TAG.
Inorganic phosphate is an essential nutrient because it is required for the biosynthesis of nucleotides, phospholipids and metabolites in energy metabolism. During phosphate starvation, phosphatases play a major role in phosphate acquisition by hydrolyzing phosphorylated macromolecules. In Saccharomyces cerevisiae, PHM8 (YER037W), a lysophosphatidic acid phosphatase, plays an important role in phosphate acquisition by hydrolyzing lysophosphatidic acid and nucleotide monophosphate that results in accumulation of triacylglycerol and nucleotides under phosphate limiting conditions. Under phosphate limiting conditions, it is transcriptionally regulated by Pho4p, a phosphate-responsive transcription factor. In this review, we focus on triacylglycerol metabolism in transcription factors deletion mutants involved in phosphate metabolism and propose a link between phosphate and triacylglycerol metabolism. Deletion of these transcription factors results in an increase in triacylglycerol level. Based on these observations, we suggest that PHM8 is responsible for the increase in triacylglycerol in phosphate metabolising gene deletion mutants.
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