بر سطح هموگلوبين گليكوزيله در بيماران ديابت نوع 2 C بررسي اثرفارماكولوژيك ويتامين

Effect of pharmacologic doses of vitamin C on glycosylated hemoglobin in type 2 diabetic patients

Introduction: Formation of end-glycation products is one of the major causes of chronic diabetes complications. Although there is some evidence that vitamin C inhibits protein and hemoglobin glycosylation in healthy individuals, its effect on diabetic patients is still being debated. The aim of this clinical trial was to examine the pharmacologic effect of vitamin C on hemoglobin A1c (HbAlc) and fasting blood sugar (FBS plasma levels) in diabetic patients. Materials and Methods: For this purpose 53 (8 male, 45 female) type 2 diabetic patients who had FBS <250 mg/dL were selected for the study. The age range was 37-70 years with a mean of 52.8±10 years. Patients were given 1g vitamin C per day for 3 months. Changes in body weight, FBS, and HbAlc level were compared before and after therapy. FBS was measured by the enzymatic glucose oxidase method (normal range: 75-110 mg/dL) and HbAlc was assayed according to WHO calorimetric method with a normal range of 2.5-4 miumol/g Hb%. Results: The mean FBS level was 185±43.9 mg/dL at the beginning and 176.5± 48.7 mg/dL at the end of study. The mean FBS level changes during study was -8.9±40.2 mg/dL, which was not significant (p>0.05). The mean HbA1c level at the beginning was 4.9± 0.9, at the end 4.7±1, with a mean change of range -0.2±0.9 miumol/gHb%, which was not significant (p>0.05). Also mean body weight changes were not significant during study (p>0.05). The decrease in level of HbAlc from 1 to 15%, shown in 49% of patients was related significantly to decreased weight (p<0.001) and in the 26% with most decreased HbAlc levels (10-15%), it was related also to decreased FBS (p.0.05). Conclusion: According to these results, decreased HbAlc level was due to weight loss and better glucose control rather than vitamin C effects. Therefore vitamin C consumption for prevention of type 2 diabetes complications by inhibition of protein glycosylation is not recommended.