Aim of study: to determine the pathogenetic factors that have an impact on the development of diabetic myopathy in children with DM1, to investigate the structure of the factors. The observation group included 136 children 14.3 ± 0.3 years old who have been suffering from DM1 for 1 to 10 years. Diagnosed diabetic myopathy in 45 (33.1%) patients (19 (24.4%) boys and 25 (44.8%) girls). By factor analysis, 5 factors were identified that are of leading importance in the pathogenesis of the development of diabetic myopathy in children with DM1. These factors accounted for 73.33% of the total dispersion. The first rank place was represented by the group factor (nitrotyrosine and homocysteine), which accounted for 19.54% of the total dispersion; interpreted as a factor of "oxidative stress". The second rank place was represented by the content of triglyceride in the blood serum and the level of the triglyceride-glucose complex, which amounted to 16.69% of the total dispersion; interpreted as "insulin resistance factor". The third rank place was interpreted as "the state of peripheral blood supply", which accounted for 13.93% of the total variance, and included the indicators of the ankle-brachial index before and after exercise stress. The fourth rank place was interpreted as an "anamnestic factor", which accounted for 12.04% of the total dispersion, and included three risk factors: age, sex of the patient, and duration of DM1. The fifth factor ("inflammation factor") included the indicators of glycosylated hemoglobin and interleukin-6, and demonstrates the development of chronic low-level inflammation against the background of hyperglycemia. Thus, using factor analysis, we determined that oxidative stress, insulin resistance, impaired peripheral circulation, duration of diabetes mellitus, female sex, chronic hyperglycemia, increased activity of proinflammatory cytokines had a priority effect on the pathogenesis of diabetic myopathy. We have formed a factorial model that will optimize the diagnosis of diabetic myopathy, improve approaches to its therapy and prevention, identifying among children with DM1 the risk group for the development and progression of this complication.

Background. The purpose was to determine the pathogenetic role of oxidative stress in the development of diabetic myopathy in children with diabetes mellitus. Materials and methods. The study included 60 children with type 1 diabetes mellitus (DM1), aged 11 to 17 years. Group 1 included 20 patients with a duration of disease less than 1 year. Group 2 consisted of 20 patients with a duration of diabetes from 1 to 5 years. Group 3 was formed of 20 kids with the duration of diabetes over 5 years. The control group consisted of 20 apparently healthy children. All children underwent the ske­letal muscle index determination, ultrasound examination of skeletal muscles, and determination of the level of creatine phosphokinase, homocysteine, and nitrotyrosine in the blood serum. Results. According to the conducted ultrasound diagnostics, the DM1 children were found to present a decrease in the mass of skeletal muscles due to a reduced muscle thickness in the dynamics of the disease. It was proved that hyperglycemia in children with DM1 resulted in the significant oxidative stress confirmed by an increase in the blood serum content of homocysteine and nitrotyrosine, and damage to skeletal muscles, which was confirmed by high blood serum levels of creatine phosphokinase, started from 1 year of illness. Significant changes were found in group 3 of children, where high values of homocysteine and nitrotyrosine were determined in comparison with both the control and group 1 of the study (p < 0.05). An inverse correlation was found between the levels of homocysteine, nitrotyrosine, and the skeletal muscle index, respectively (r = –0.39 (p < 0.05); r = –0.35 (p < 0.05)), and the dependence of these indicators on the state of glycemic control. Conclusions. There is a progressively increased activity of creatine phosphokinase from 1 year of DM1, which indicated early damage to the muscle tissue in children with type 1 diabetes mellitus. One of the causes of skeletal muscle damage and the formation of diabetic myopathy in diabetic children is oxidative stress, which increased with poor glycemic control.

Background. The purpose was to determine the frequency, risk factors of the development of diabetic myopathy in children with type 1 diabetes mellitus (DM1), and to create a ma­thematical model for predicting the formation of pathology. Materials and methods. The observation group consisted of 136 children with DM1. All children underwent a comprehensive clinical, instrumental, and laboratory examination and assessment of the state of skeletal muscles to determine the risk factors for the development of diabetic myopathy. The prognostic significance of individual signs as risk factors of the development of diabetic myopathy in children with DM1 was analyzed based on calculating the relative risk (RR) index. The most significant factors included informative signs with an RR value of more than 1.0. The binary logistic regression method was used to predict the likelihood of developing diabetic myopathy. Results. The complex study showed that the development of diabetic myopathy took place in 45 (33.1 %) children. Based on the calculation of the RR index, out of 29 potential predictors, 7 risk factors were selected that can influence the development of diabetic myopathy: sex, age, duration of the disease, glycated hemoglobin level, fat mass index (FMI), ankle-brachial index, and the presence of peripheral neuropathy. A logistic regression model was constructed for individual prediction of the likelihood of developing diabetic myopathy. The classification model capacity was 90.2 %. The model sensitivity and specificity is 80.0 %, which characterizes the excellent quality of the classification of predictors and the high significance of the identified factors of the development of diabetic ­myopathy in children with DM1. Conclusions. Diabetic myopathy is a common complication of diabetes mellitus in children and develops in 33.1 % of cases. The priority contribution of the development of diabetic myopathy in children with DM1 is the state of glycemic control, the duration of diabetes mellitus, the patient’s age, sex, the presence of diabetic peripheral polyneuropathy, peripheral circulatory disorders, and an increase in the IMF. The developed mathematical forecasting model allows calculating with a high probability of developing diabetic myopathy in children with diabetes mellitus and can be used to identify patients with a high risk of developing this complication for the timely implementation of diagnostic and preventive management.

The aim — to study the role of myokines in the development of insulin resistance in children with type 1 diabetes mellitus.Materials and methods. Observations involved 68 children with type 1 diabetes mellitus (DM 1), with the mean age 11 to 17 years. Depending on the glycemic controllevel, patients were divided into 3 research groups. The control group consisted of 20 relatively healthy children. Muscle mass, the skeletal muscles index, fat mass and the percentage of fat in the bodywere determined in all patients. The Lovett’s test was used to assess the loss of muscle strength; evaluation of insulin resistance was made based onthe triglyceride­glucose index (TYG). Levels of myostatin, irisin, interleukins ­6 and ­13were measured in blood serum.Results and discussion. It has been established that with deterioration in the level of glycemic controlin DM 1 children, the component redistribution of body composition took place with an increased fat mass proportionand decreased muscle mass. This resulted in the reduced insulin-mediatedabsorption of glucose, that was confirmed by the significant increase in TYG level compared to control group. The analysis of cytokines in the blood serum showed a significant increase in the level of myostatin and interleukin­6 compared with the control group and the tendency to increased levels of the interleukins ­13 and the level of irisin in the blood serum in pediatric patients with DM 1. The increased levels of myostatin in DM 1childrenassociated with an increase in the triglycerides content (r = 0.44, p < 0.05) and raised TYG index (r = 0.33, p < 0.05), testifying theclose correlation between the high myostatin levels and the development of insulin resistance.Conclusions. In children with diabetes mellitus, the reduction of muscle strength and muscle mass take place with a deterioration in the state of glycemic control, accompanying by the development of insulin resistance. The violation of myokines synthesis,along with the chronic hyperglycemia and diabetic myopathy, plays the leading role in the formation of insulin resistance in pediatric patients with DM 1. It is manifested by the increased production of myostatin and interleukin­6 in the absence of activation of irisin and interleukin­13synthesis.

The purpose of the study: to study the amount of irizin in the blood serum of children with Type 1 diabetes considering the duration of clinical course and determine the role of irizin in diagnosing the diabetic myopathy. The study included 90 children with Type 1 diabetes (T1D) (average age 13,7±0,4 years old). Depending on the duration of the disease, 3 groups were formed: 1 group — 26 children under 1 year with T1D; group 2 — 27 children — duration of T1D from 1–5 years; group 3 — 37 children with T1D duration more than 5 years. The control group included of 25 conditionally healthy children of a representative age and gender. All children were evaluated for their muscle and fat mass and their indices, ultrasound examination of skeletal muscles, and determination of irisin levels in the blood serum by ELISA. It was established that with increasing durations of T1D there was a redistribution of the component body composition in the form of a decrease in the specific the muscle mass and an increase in the percentage of fat mass, as well as changes in the ultrasound pattern of skeletal muscles characterized by a decrease in the thickness of the muscle fibers, a infraction of the normal architecture of muscle and increased echogenicity of muscle bundles. It was established that in the first years of the disease, the decrease in muscle mass was accompanied by a decrease in the level of irisin, whereas with the prolonged course of T1D there was an increase in it, which was accompanied by loss of muscle mass and infraction of the architecture of skeletal muscles. Thus, increasing the level of irisin can be used as an additional marker for the development of diabetic myopathy.