U Cakatay1. 1. Istanbul University, Istanbul Faculty of Medicine, Central Laboratory of Biochemistry, Capa, 34390 Istanbul, Turkey. cakatay@yahoo.com
Abstract
AIM: In order to examine the influence of oxidative stress on protein oxidation, type 2 diabetic patients without clinical evidence of complications, either in good or poor glycaemic control, were studied. METHODS: Plasma protein carbonyl (PCO), total thiol (T-SH), and advanced oxidation protein products (AOPP) levels as markers of protein oxidation, and lipid hydroperoxide (LHP) levels as markers of lipid peroxidation were determined. Glycated haemoglobin (HbA1c) levels were used as an index of glycaemic control. The subjects were divided into two groups according to their HbA1c level at inclusion as follows: good HbA1c<=7%, and poor HbA1c > 7%. RESULTS: Plasma PCO and AOPP levels of diabetic patients with poor glycaemic control were increased significantly compared with those of the diabetic patients with good glycaemic control. The decreased plasma T-SH level in the diabetic patients with poor glycaemic control was not statistically significant. On the other hand, plasma LHP levels were increased significantly in the diabetic patients with poor GC compared with those of the diabetic patients with good glycaemic control. CONCLUSION: This study supports the hypothesis that poor glycaemic control is an important factor in generation of increased protein oxidation in type 2 diabetic patients clinically free of complications. Increase in plasma PCO, AOPP, and LHP levels in the diabetic patients with poor glycaemic control may contribute to the development of diabetic complications.
AIM: In order to examine the influence of oxidative stress on protein oxidation, type 2 diabeticpatients without clinical evidence of complications, either in good or poor glycaemic control, were studied. METHODS: Plasma protein carbonyl (PCO), total thiol (T-SH), and advanced oxidation protein products (AOPP) levels as markers of protein oxidation, and lipid hydroperoxide (LHP) levels as markers of lipid peroxidation were determined. Glycated haemoglobin (HbA1c) levels were used as an index of glycaemic control. The subjects were divided into two groups according to their HbA1c level at inclusion as follows: good HbA1c<=7%, and poor HbA1c > 7%. RESULTS: Plasma PCO and AOPP levels of diabeticpatients with poor glycaemic control were increased significantly compared with those of the diabeticpatients with good glycaemic control. The decreased plasma T-SH level in the diabeticpatients with poor glycaemic control was not statistically significant. On the other hand, plasma LHP levels were increased significantly in the diabeticpatients with poor GC compared with those of the diabeticpatients with good glycaemic control. CONCLUSION: This study supports the hypothesis that poor glycaemic control is an important factor in generation of increased protein oxidation in type 2 diabeticpatients clinically free of complications. Increase in plasma PCO, AOPP, and LHP levels in the diabeticpatients with poor glycaemic control may contribute to the development of diabetic complications.
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