Diabetes mellitus is associated with hyperglycemia and with accelerated non-enzymatic glycation, increased oxidative stress and free radical production. The aim of the present study was to evaluate the levels of proteins glycation and oxidation parameters, compare them between poorly and well controlled children with type 1 diabetes mellitus, and determine the impact of glycemic control on these parameters. Blood and serum were obtained from 81 patients with type 1 diabetes mellitus (DM1) (20 patients had long-term good glycemic control [GGC], 61 patients had long-term poor glycemic control [PGC]). Thirty-one healthy children were used as controls. Fructosamine (FAM) was determined by a spectrophotometric method, HbA1c was measured by LPLC, serum advanced glycation end-products (s-AGEs) were determined fluorimetrically, and advanced oxidation protein products (AOPP) were measured spectrophotometrically. We observed significantly higher FAM, HbA1c, s-AGEs and AOPP levels in the patients with DM1 compared with controls, and significantly higher FAM, HbA1c and sAGEs levels in the PGC group compared with the GGC group. AOPP was higher in the PGC group than in the GGC group, but not significantly. In the PGC group we observed significant correlations between HbA1c and HDL-C (r = -0.306, p = 0.01), HbA1c and s-AGEs (r = 0.486, p < 0.001), and HbA1c and AOPP (r = 0.447, p < 0.01). s-AGEs significantly correlated with triacylglycerols (TAG) (r = 0.537, p < 0.001) and AOPP with HDL-C (r = -0.336, p < 0.05), TAG (r = 0.739, p < 0.001) and s-AGEs (r = 0.577, p < 0.001). In conclusion, our results showed both glycative and oxidative stress are increased in the PGC diabetic group compared with controls, they are linked with glycemic control, and probably contribute to the development of diabetic complications. We suggest that the measurement of not only HbA1c but also s-AGEs and AOPP may be useful to predict the risk of development of diabetic complications.

The present study investigates the relationship between diabetes metabolic control represented by levels of HbA1c, early glycation products-(fructosamine (FAM)), serum-advanced glycation end products (s-AGEs), lipoperoxidation products (LPO), advanced oxidation protein products (AOPP) and circulating TGF-β in young patients with DM1. The study group consisted of 79 patients with DM1 (8–18 years). 31 healthy children were used as control (1–16 years). Baseline characteristics of patients were compared by Student's t-test and nonparametric Mann-Whitney test (Statdirect), respectively. The correlations between the measured parameters were examined using Pearson correlation coefficient r and Spearman's rank test, respectively. A P value < 0.05 was considered as statistically significant. HbA1c was measured by LPLC, s-AGEs spectrofluorimetrically, LPO and AOPP spectrophotometrically and TGF-β by ELISA. Our results showed that parameters of glycation and oxidation are significantly higher in patients with DM1 than in healthy control. The level of serum TGF-β was significantly higher in diabetics in comparison with control: 7.1(3.6; 12.6) versus 1.6(0.8; 3.9) ng/mL. TGF-β significantly correlated with age and duration of DM1. There was not found any significant relation between TGF-β and parameres of glycation and oxidation. However, these results do not exclude the association between TGF-β and the onset of diabetic complications.

Glycation and oxidative stress lead to formation of compounds that have several biological effects and contribute to the development of the complications of diabetes mellitus. All steps of glycoxidation generate oxygen free radicals, some of them in common with lipid peroxidation pathways. Some oxidation or lipid peroxidation products may bind to proteins and amplify glycoxidation-generated lesions. The aim of this study was to measure glycation and lipid peroxidation parameters and examine the relationship between them in patients with type 1 diabetes mellitus (DM1) with (+DC) and without (-DC) diabetic complications. Fifty patients with DM1 aged from 7-19 years and with duration of DM1 (DD) at least 5 years were included. Twenty-four patients were -DC and 26 were +DC. Twelve healthy children formed a control group. There were significantly higher values of fructosamine (FAM), HbA(1c), serum advanced glycation endproducts (s-AGEs) and lipid peroxides (LPO) in the +DC group compared with -DC, and significantly higher values of HbA(1c), FAM and LPO in both diabetic groups than in controls. The s-AGEs level in the -DC group was similar to that in controls. In the total diabetic group, regardless of DC, there was a significant negative correlation between LPO and HDL-C (r = -0.379; p <0.05), and a positive correlation between LPO and triacylglycerol (TAG) (r = 0.852; p <<0.05), FAM (r = 0.414; p <0.05) and s-AGEs (r = 0.454; p <0.05). In the +DC group LPO correlated negatively with HDL-C (r = -0.392, p <0.05) and positively with TAG (r = 0.848; p <<0.05), FAM (r = 0.457; p = 0.02), and s-AGEs (r = 0.516, p = 0.02), whereas in the -DC group LPO correlated only with HDL-C (r = -0.441; p = 0.03) and TAG (r = 0.769; p <<0.05). We demonstrated a linkage between enhanced formation of AGEs and lipid peroxidation products and the presence of diabetic complications. Thus, the overproduction of glycation and lipid peroxidation products may take part in DC development as early as in childhood and adolescence.

The authors aimed to evaluate if the monitoring of serum advanced glycation end-products (s-AGEs) could help to predict a development of diabetic complications. Clinical and biochemical parameters including fructosamine (FAM), glycated hemoglobin (HbA1c) and serum AGEs were investigated in children and adolescents with 1 type diabetes with (+DC) and without (–DC) complications. FAM levels (in mmol/l) were significantly elevated in +DC diabetic group compared to –DC one (3.043±0.459 vs. 2.614±0.430; p<0.001) or to controls (3.043±0.459 vs. 1.620±0.340; p<0.001) as well as in –DC compared to controls (2.614±0.430 vs. 1.620±0.340; p<0.001). HbA1c (in %) were significantly elevated in +DC diabetic group compared to –DC one (10.48±1.83 vs. 8.41±1.19; p<<0.001) or to controls (10.48±1.83 vs. 5.0±0.38, p<<0.001) and also in –DC compared to controls (8.41±1.19 vs. 5.0±0.38; p<0.001). Serum AGEs levels (in A. U.) were significantly higher in +DC group than in – DC (73.0±14.09 vs. 65.8±9.05; p<0.05) and in group +DC than in controls (73.0±14.09 vs. 60.17±13.78; p<0.05), whereas there was no difference between –DC and controls. FAM correlated with HbA1c in both diabetic groups (+DC: r=0.374; p<0.05; –DC: r=0.719; p<0.001), but not in controls. Serum AGEs were correlated with HbA1c (r=0.478; p=0.003) in +DC, but not in –DC or controls. Enhanced serum AGEs levels show that they could be not only an attendant phenomenon of microangiopathies, but also a predictor of their development.

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