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Lipids and lipid peroxidation in diabetes mellitus with complications

Journal Name:

  • Indian Journal of Basic & Applied Medical Research

Publication Year:

  • 2014

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Abstract (2. Language): 
Diabetes Mellitus comprises a group of heterogenous metabolic disorders that share a phenotype of hyperglycemia. Due to hyperglycemia, the metabolic disorders are progressed to lead into a endothelial dysfunction, atherosclerosis and alterations in the large blood vessels. Dyslipidemia is one of the important pathogenic factor for micro (nephropathy) and macro vascular diseases (Cardiac complications). Hyperglycemia is widely known cause of enhanced plasma free radical concentrations of oxidative stress. Malondialdehyde (MDA) is the important marker for the oxidative stress. In the present study, an attempt was made to study the influence of dyslipidemia during the complications of Diabetis Mellitus and how the lipid peroxidation will induce the damage to various organs in diabetics. During the study, 120 Type- 2 Diabetic patients were selected under test group and estimated the parameters like Fasting Plasma Glucose, Urea, Creatinine, Triglycerides, Total Cholesterol, HDL, LDL, VLDL fractions of Cholesterol by standard kit methods and Malondialdehyde by TBA reaction using spectrophotometer and compared the values with age, sex matched controls number 50. It was observed that a significant increase in the TG (P>0.001) and Total Cholesterol (P>0.001), VLDL (P> 0.001) during all the three complications due to Diabetes Mellitus and lower levels of HDL cholesterol was observed. LDL Cholesterol was elevated significantly during the complications of Dermatological, Ophthlmic and Nephrological diseases. Malondialdehyde elevation seen in above disease conditions indicating the increased free radical production. Enhanced MDA has been proposed to be one of the mechanism that influenced the rapid progression of diabetic vasculopathy. The peroxidative lipid damage can increase coagulability, alter phospholipid organisation and reduce the survival of cell, due to the formation of advanced glycation end products (AGEs), which might generate toxic reactive oxygen species.
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