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.

Spina bifida is a developmental defect of the spinal cord and / or spine that results from abnormal closure of the embryonic neural tube. Many factors have been described to determine the risks of developing this pathology, but the incidence of the defect is still high. 61 % of patients with Spina bifida have neurogenic bladder dysfunction based on intravesical hypertension, which contributes to reverse urethral flow and bladder-uretero-renal reflux associated with chronic inflammatory and obstructive urinary tract disease. In 25–50 % of patients with Spina bifida, urological pathology is complicated by the development of chronic kidney disease, which significantly reduces the quality of life of these patients. In some types of Spina bifida, urological symptoms may be prominent or even isolated and may indicate the presence of the malformation. Therefore, early diagnosis of Spina bifida and timely prophylactic and therapeutic measures are of particular importance.

Introduction: Insulin-like growth factor-1 (IGF-1) is a potent mitogen for glomerular mesangial cells which can stimulate cell migration and the production of fibronectin, proteoglycan, and type IV collagen, thereby promoting the development of the chronic kidney disease (CKD) in patients with diabetes. Objectives: The aim of the study was to assess the associations between serum levels of IGF-1 and insulin-like growth factor-binding protein-3 (IGFBP-3) and CKD in diabetic patients. Patients and Methods: We investigated 102 Belarusian men and women with diabetes type 2 aged 56.67±0.81 years. Control group included 68 healthy people the same age. We estimated GFR with the use of the CKD-EPI creatinine-cystatin C equation to determine eGFRcr_cys. Serum total IGF-1 and IGFBP-3 levels were measured using immunoradiometric assay (IRMA) (Beckman Coulter, Czech Republic s.r.o.). Results: Patients with diabetes had significantly lower level of IGF-1 than controls. However, IGFBP-3 levels were similar in the two groups. Diabetic patients with CKD had significantly higher levels of IGF-1 and IGFBP-3 than diabetic patients without CKD (P=0.0031). However, according to multivariate analysis, only IGF-1 and cystatin C were associated with renal impairment. In detail, the odds of having eGFR<60 mL/min/1.73 m² increased with rising IGF-1 levels (OR: 1.025, [CI 1.002-1.048]). Conclusion: Our study revealed that higher serum IGF-1 levels were positively associated with CKD in patients with diabetes. We suggest that IGF-1 might be a predictor of CKD in patients with diabetes. Further research is necessary to confirm the observed this association and to detect the causal relations.

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.

Introduction: A Diabetes mellitus (DM) and chronic kidney disease (CKD) are two chronic non-communicable diseases that have exceeded epidemic thresholds in all countries of the world. The problem of early diagnosis, prevention and treatment of CKD continues to be relevant for modern medicine, and assessment of the severity of CKD and associated cardiovascular complications is of great practical importance for primary and secondary prevention. Objectives: The aim of the study was to assess the role of proinflammatory cytokines, chemokines and growth factors in progression of CKD in patients with DM. Patients and Methods: We screened 155 type 2 DM patients aged 65.00 (55.00-71.00) years. Control group included 21 healthy people with the same age. Renal function was assessed based on the levels of serum creatinine, cystatin C, estimated glomerular filtration rate (eGFR), which was calculated according to the CKD-EPI (chronic kidney disease epidemiology collaboration) equation, and albuminuria, which was assessed as albumin/creatinine ratio (A/C). The analysis of serum and urine biomarkers was carried out by enzyme immunoassay using commercial test systems. Results: Patients with DM had significantly higher levels of proinflammatory cytokines in comparison with the control group. The levels of interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), vascular endothelial growth factor A (VEGF-A), fibroblast growth factor-23 (FGF-23), regulated upon activation, normal T cell expressed and presumably secreted (RANTES), MIG, CRP, kidney injury molecule-1 (KIM-1) and homocysteine gradually increased with decreasing GFR. According to the results of univariate linear regression analysis, there were significant relationships between the levels of VEGF-A, FGF-23, RANTES, tumor necrosis factor alpha (TNF-alpha), MIG, CRP, hs-CRP, IL-6 and renal function. By multiple linear regression analysis adjusted for confounding factors, serum creatinine was significantly correlated with FGF-23 (β=0.40, P<0.001) and Il-6 (β=0.29, P<0.001). Conclusion: Our study demonstrated the important role of growth factors and proinflammatory cytokines in the development and progression of CKD in DM. However, despite these data, the pathogenesis of diabetic changes in the kidneys remains not fully understood and, in order to clarify the possibility of pathogenetic influences on the progression of diabetic nephropathy, it is necessary to study various aspects of its development, including genetic factors.

The aim of this randomized comparative study was to assess renal and metabolic effects of vildagliptin in insulin-treated type 2 diabetes (T2DM) patients without overt chronic kidney disease. We randomized 47 insulin-treated non-proteinuric patients with satisfactory controlled T2DM and estimated glomerular filtration rate (eGFR) ≥ 60 mL/min/1.73m 2 either to continue insulin therapy (control) or to receive combined insulin-vildagliptin treatment (VIG group). We assessed eGFR using serum creatinine (eGFRcreat), cystatin C (eGFRcys), and both (eGFRcreat-cys), and urinary creatinine-adjusted excretion of albumin (UACR), type IV collagen (uCol IV/Cr), and neutrophil gelatinase-associated lipocalin (uNGAL/Cr) at baseline and after 6 months of treatment. Study groups were comparable in terms of age and sex (60.1 ± 6.1 years and 42.9% men in control group vs. 60.8 ± 5.2 years and 39.1% in VIG group). After 6 months of treatment, there were no significant changes in main assessed parameters in control group. VIG group demonstrated significant decrease in HbA1c, diastolic blood pressure, frequency of hypoglycemia, and high-sensitivity C-reactive protein level as compared to the changes in control group. While eGFRcreat, UACR, and uNGAL/Cr showed no significant changes after vildagliptin addition, eGFRcys, eGFRcreat-cys, and uCol IV/Cr changed significantly in comparison with control group (+7.0% [3.7;13.3]; +5.1% [1.4;8.5]; -32,8% [-55.8;-24.4], respectively, p < 0.01 each). Correlation and regression analysis revealed glucose-independent pattern of these changes. Addition of vildagliptin to ongoing insulin therapy in patients with T2DM was associated with a reduction in uCol IV/Cr and an increase in eGFRcys and eGFRcreat-cys, independent of T2DM control parameters.