BACKGROUND: There exist several reports demonstrating enhancement in oxidative stress in diabetic patients; however, serial and comprehensive measurement of oxidative stress parameters in newly diagnosed diabetic patients is not yet reported. We measured the oxidative stress parameters in diabetic patients serially from the time of diagnosis and after starting treatment to study their association with glycaemia, insulin resistance and β-cell function. METHODS: Fifty-four newly diagnosed diabetic patients were studied at diagnosis and 4 and 8 weeks after initiating anti-hyperglycaemic treatment. Oxidative stress parameters included activity of antioxidant enzymes, concentration of antioxidant molecules and damage markers. Oxidative stress score was computed as a collective measure of oxidative stress to interpret total oxidative stress state. Association of changing glucose levels with changing oxidative stress parameters over 8 weeks and association of oxidative stress score with insulin resistance and β-cell function was analysed by homeostasis model assessment (HOMA-IR and HOMA-β, respectively). RESULTS: Eight weeks of treatment improved HbA1C from 9.8 ± 2.1 to 7.7 ± 1.0%. There was a significant increase in oxidative stress in diabetic patients [23.8 (95% CI 20.0, 27.6)] compared with non-diabetic subjects [-1.2 (-3.4, 0.9)] (p < 0.001). Non-diabetic subjects showed a stable status over 8 weeks. Improvement in hyperglycaemia in diabetic patients was associated with an improvement in oxidative stress parameters irrespective of the anti-diabetic treatment received. Oxidative stress score fell after 8 weeks and was significantly associated with an improvement in HOMA-β (standardized β = -0.38, p < 0.01) but not with HOMA-IR. CONCLUSIONS: Controlling hyperglycaemia in diabetic patients alleviates oxidative stress within 8 weeks of treatment, and improvement in oxidative stress parameters was related to an improved β-cell function.
BACKGROUND: There exist several reports demonstrating enhancement in oxidative stress in diabeticpatients; however, serial and comprehensive measurement of oxidative stress parameters in newly diagnosed diabeticpatients is not yet reported. We measured the oxidative stress parameters in diabeticpatients serially from the time of diagnosis and after starting treatment to study their association with glycaemia, insulin resistance and β-cell function. METHODS: Fifty-four newly diagnosed diabeticpatients were studied at diagnosis and 4 and 8 weeks after initiating anti-hyperglycaemic treatment. Oxidative stress parameters included activity of antioxidant enzymes, concentration of antioxidant molecules and damage markers. Oxidative stress score was computed as a collective measure of oxidative stress to interpret total oxidative stress state. Association of changing glucose levels with changing oxidative stress parameters over 8 weeks and association of oxidative stress score with insulin resistance and β-cell function was analysed by homeostasis model assessment (HOMA-IR and HOMA-β, respectively). RESULTS: Eight weeks of treatment improved HbA1C from 9.8 ± 2.1 to 7.7 ± 1.0%. There was a significant increase in oxidative stress in diabeticpatients [23.8 (95% CI 20.0, 27.6)] compared with non-diabetic subjects [-1.2 (-3.4, 0.9)] (p < 0.001). Non-diabetic subjects showed a stable status over 8 weeks. Improvement in hyperglycaemia in diabeticpatients was associated with an improvement in oxidative stress parameters irrespective of the anti-diabetic treatment received. Oxidative stress score fell after 8 weeks and was significantly associated with an improvement in HOMA-β (standardized β = -0.38, p < 0.01) but not with HOMA-IR. CONCLUSIONS: Controlling hyperglycaemia in diabeticpatients alleviates oxidative stress within 8 weeks of treatment, and improvement in oxidative stress parameters was related to an improved β-cell function.