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Inadequate nutrition prevents patients with type 2 diabetes (T2DM) from achieving target values of glycemic and non-glycemic parameters. Aim: to evaluate metabolic effects of the balanced diet including specialized nutrition (SN). Material and methods: the randomized clinical trial included 60 patients with type 2 diabetes treated with a double combination metformin + glibenclamide, who were divided into 2 groups. Patients in the treatment group received SN Glucerna SR which replaced the main meal; the comparison group of patients were on a natural low-calorie diet. Changes in glycemic and non-glycemic parameters were evaluated in 12 weeks. Results: SN improves glycemic control without correction of the background antidiabetic therapy. Thus, the treatment group demonstrated a decrease in HbA1c from 7.8 ± 1.6 to 6.7 ± 1.1%, fasting glycemia - from 7.5 ± 1.2 to 5.9 ± 0.6 mmol/l, postprandial glucose (PPG) - from 10.6 ± 1.0 to 7.5 ± 0.5 mmol /l, glycemic variability SD - from 2.0 ± 0.8 to 1.1 ± 0.6 mmol/l, and normalization of glycemic pattern (p < 0.05). SN contributed to improvement of the lipid profile (p < 0.05). Conclusions: SN in patients with type 2 diabetes and visceral obesity is associated with positive dynamics of metabolic parameters. Elimination of postprandial hyperglycemia induces a decrease in glycemic variability, minimizing the progression of type 2 diabetes.

Diabetes mellitus (DM) is a serious medical and social problem. The prevalence of diabetes has been steadily increasing in all countries, where 95% are patients with type 2 diabetes. According to the International Diabetes Federation, in 2014, the number of patients with type 2 diabetes was 387 million, or every 12th inhabitant of the planet. By 2035, the number of patients with type 2 diabetes could increase to 592 million people [1]. Global trends in diabetes incidence rates are also observed in Russia. According to the national register, there are 8 million diabetic patients in Russia, or approximately 5% of the total population, whereas 90% of them are patients with type 2 diabetes. By 2025, the number of patients is expected to increase to 13 million people. The number of registered patients is usually 2-3 times less than the real number. [2, 3] The greatest input in the number of diabetic patients is made by the increase in the number of type 2 diabetes patients in older age groups.

The article is an overview of the prevalence, mechanisms of development, diagnosis and treatment of diabetic neuropathy as a complication of diabetes. It also tells about the pathogenetic aspects of treatment of diabetic polyneuropathy.

Oxidative stress is the pathogenetic basis for the progression of T2DM. It is important to evaluate antioxidant properties of testosterone medications used for the management of male hypogonadism (a comorbidity of T2DM). Aim: to evaluate antioxidant properties of testosterone hormone replacement therapy (THRT) in patients with type 2 diabetes. Material and methods: the randomized (1:1) clinical trial included 108 patients with type 2 diabetes, visceral obesity and hypogonadism. The treatment group received THRT for 12 months. The changes in metabolic (glycemic and non-glycemic) parameters and activity of antioxidant protection enzymes - superoxide dismutase (SOD) and glutathione peroxiase, (GPO), were evaluated. The ΔOxS index was suggested to characterize the changes in oxidative stress. Results: THRT was associated with improved metabolic and antioxidant status. Increased SOD and GPO activity against a background of THRT was 32.4 ± 5.6 U/l and 580 ± 68 U/ml, respectively (p < 0.05). ΔOxS was characterized by positive changes only in the treatment group, indicating a decrease in oxidative stress during THRT. Conclusions: in patients with visceral obesity and T2DM, THRT contributed to improvement in metabolic parameters and elimination of oxidative stress and glucose-lypo-toxicity, and that could potentially reduce the risk of progression of type 2 diabetes and its complications.

The article tells about generalized Russian experience in the treatment of patients with diabetes and heart failure. The role of medicines affecting various links in the pathogenesis of diabetes mellitus in patients with concomitant cardiovascular diseases is deminstrated. The role of taurine as the optimum addition to glucose-lowering therapy in this group of patients is emphasized.

The role of hyperglycemia as an independent predictor of adverse course and prognosis of acute coronary syndrome (ACS) in patients with diabetes mellitus (DM) and without it [1] can hardly be overestimated. This relationship is thoroughly covered in the literature [2-- 13], and the discussions on the subject are underway. A simple summation of risks results in higher than expected rates of morbidity and mortality from CAD in DM patients, demonstrating a direct effect of hyperglycemia on the atherosclerotic process [14--16]. It is worth noting that in patients without DM hyperglycemia is associated with worse clinical outcomes and higher mortality from all causes compared with patients suffering from diabetes mellitus [17--21]. Increased blood sugar levels at the time of admission are usually seen as a reaction to stress in acute condition, but in some cases may serve as a marker of an existing though not yet diagnosed type 2 diabetes or impaired glucose tolerance (IGT) [22]. According to observational studies, hyperglycemia occurs in 32--38% of patients in hospitals [23, 24], 41% of severe patients with acute coronary syndrome[25], 44% of patients with heart failure [25] and 80% of patients after coronary intervention [26, 27].

Obesity increases the risk of diabetes mellitus type 2 due to the development of insulin resistance. Therapy for diabetes mellitus type 2 is limited by a relatively small amount of knowledge on the mechanisms of insulin resistance, despite the availability of several scientifically valid hypotheses about its origin. These theories focus on inflammation, mitochondrial dysfunction, hyperinsulinemia and lipotoxicity as playing the key role in the process. Absence of a general pathogenic mechanism of insulin resistance which combines all of the theories attracts attention to the issue. At the same time, none of the mentioned concepts or views resulted in an improvement or higher efficiency of treatment for diabetes mellitus type 2.