Diabetic nephropathy (DN) is a serious complication of diabetes mellitus (DM), which increases morbidity and mortality. Accumulated evidence, mostly experimental ones that DPP-4 inhibitors have non-glycemic tissue effects including renal protection. Clinical data confirming these effects are insufficient. This makes it relevant to study the influence of iDPP-4 on the renal function in patients with Type 2 diabetes.To study the effects of iDPP vildagliptin on glycemic, metabolic and renal parameters in patients with type 2 diabetes with CKD 1–2 receiving insulin therapy 44 patients were randomized to continue therapy with insulin or insulin + vildagliptin at a dose of 50 mg/day, with the evaluation of results in 6 months.In group of vildagliptin therapy a significant decrease of HbA1c, postprandial glycemia, diastolic blood pressure, HOMA-IR, insulin demand and a reduction in the frequency of hypoglycemia occurred. The positive dynamics of indicators of glomerular functions of the kidney were noted in this group - a significant reduction in albuminuria and a significant increase in eGFR by cystatin C and decreased urinary excretion of type IV collagen. The findings suggest the positive effect of vildagliptin on metabolic status and indicators of glycaemia and hemodynamics as earlier confirmed in clinical studies and the ability of vildagliptin independent from glycemic effects to slow the development of glomerular dysfunction in patients with type 2 diabetes and the initial manifestations of DN.

Among existing genetic and non-genetic models of obesity, the most widely used are the models of diet-induced obesity in rodents due to their relatively easy reproducibility and similarities to human pathogenesis of obesity. Within this review, we provide the analysis of diet-induced obesity models in rats, highlight attractive strengths as well as disadvantages of high-fat diets, fat or sugar choice diets, “cafeteria diets”, and “western diet”. Potential obesogenic mechanisms of the discussed models are analyzed. The directions of further studies required for an increase in reproducibility of experimental diet-induced obesity are proposed.

The present review summarizes the results of global studies and assesses contribution of hyperglycemia towards formation of neurologic complications in diabetic patients. Hyperglycemia is believed to play a leading role in the formation of neurological complications in diabetes mellitus. However, the achievement of normalization of glycemia level does not ensure the cessation of their development and progression, which indicates a lack of knowledge about the pathogenetic relationships in diabetic neuropathy. Limited understanding of these issues entails the absence of treatment options that effectively affect the course of this complication. Based on the analysis of experimental and clinical studies of recent years, data on the molecular-biological relationships of hyperglycemia with the formation of neurological complications in diabetes mellitus are summarized. The influence of the oxidative and nitrosative stress, advanced glycation end products, the activation of the polyol and hexosamine pathways on the state of the nerve fiber is analyzed. The data on molecular mechanisms of development of diabetic neuropathy are contradictory. On the basis of recent experimental and clinical data we review possibilities for pathogenetic therapy. The problem of oppositely directed effects of treatment is discussed. Clinical rationale is given for declared direction of further studies.

Recently, inflammatory and regulatory mechanisms that are involved in the onset and progression of angiopathies in diabetes mellitus (DM), including diabetic kidney disease (DKD), have been studied. In this study, we assessed the levels of fibroblast growth factor-23 (FGF-23) and inflammatory markers in patients with type 2 DM and different stages of chronic kidney disease (CKD). We investigated 64 patients with type 2 DM aged 34-84 years. The results showed significant changes in the levels of FGF-23, tumour necrosis factor alpha (TNF-alpha), C-reactive protein (CRP), high-sensitivity C-reactive protein (hsCRP), and interleukin-6 (IL-6) with the progression of CKD in patients with type 2 diabetes. Multiple regression analysis demonstrated the presence of an independent interconnection between serum levels of FGF-23 and creatinine.