Background. The aim was to establish the features of hemodynamic and metabolic parameters in obese patients with true and pseudo-resistant arterial hypertension (AH). Material and methods. The study included 200 patients with uncontrolled AH and obesity. Patients were initially prescribed dual antihypertensive therapy. Those patients who did not reach target blood pressure (BP) levels after 3 months on dual therapy were additionally prescribed a third antihypertensive drug. Of the 98 patients who were assigned to triple therapy, 48 patients did not reach target BP (27 patients had pseudo-resistant and 21 patients had true resistant AH). These patients were additionally prescribed a fourth antihypertensive drug (spironolactone). The effectiveness of the treatment was evaluated 6 months after the start of antihypertensive therapy. Results. After 6 months of therapy, unlike patients without resistance, individuals with resistant AH had more pronounced cardiovascular remodeling and metabolic disorders, disbalance of oxidative stress-antioxidant protection, proinflammatory activity and higher activity of the renin-angiotensin-aldosterone system. Patients with true resistance differed from pseudo-resistant patients by having significantly lower body mass index (BMI); in the absence of differences in BP levels, cardiovascular remodeling, lipid and carbohydrate profiles, patients with true resistance had significantly higher levels of aldosterone, higher activity of oxidative stress system, lower levels of general antioxidant protection, higher adiponectin levels, and lower leptin level. Conclusions. Obese patients with true resistance differed from pseudo-resistant patients by having significantly lower BMI, higher aldosterone levels, more pronounced imbalance of the system of oxidative stress-antioxidant protection and less pronounced adipokine imbalance.

Background: Hereditary component plays a significant role in the formation of insulin resistance (IR) - one of the pathogenetic links of arterial hypertension (AH) and type 2 diabetes mellitus (DM2). However, the genetic predisposition to IR can not be realized and does not manifest itself clinically in the absence of appropriate factors of the environment (excessive nutrition, low physical activity, etc.). Objective: The review summarizes the results of studies which describe the contribution of genetic polymorphism to the formation and progression of AH, DM2 and their comorbidity in various populations. Results: In many studies, it has been established that genetic polymorphism of candidate genes is influenced by the formation, course and complication of AH and DM2. According to research data, the modulating effect of polymorphism of some genetic markers of AH and DM2 on metabolism and hemodynamics has been established. The results of numerous studies have shown a higher frequency of occurrence of AH and DM2, as well as their more severe course with adverse genetic polymorphisms. At the same time, the role of genetic polymorphism in the formation of AH and DM2 differs in different populations. Conclusion: Contradictory data on the influence of gene polymorphisms on the formation of AH and DM2 in different populations, as well as a small number of studies on the combined effects of several polymorphisms on the formation of comorbidity, determine the continuation of research in this direction.

This is the published version of the paper.This version of the publication may differ from the final published version. Permanent repository link AbstractIn this article the problems of the prevalence of esophageal cancer and the spatial distribution of mortality rates from this disease are considered using as examples the NUTS 2 regions in six countries of Central and Eastern Europe (Austria, Germany, the Czech Republic, Poland, Slovakia and Hungary). The rates of mortality from esophageal cancer are analyzed by statistical methods and by spatial econometrics. A study is carried out of the features of the spatial distribution of the rates of mortality from esophageal cancer. It allows us to determine more and less epidemiologically affected regions and to carry out more detailed studies on the link between the mortality rates from esophageal cancer and various factors, such as the environmental situation, socio-demographic characteristics of the population, culture and nature of nutrition, the general health status of the population, the availability of resources and the level of healthcare in the region. By means of the multifactor regression model we forecast the rates of mortality from esophageal cancer, taking into account characteristics of the countries, the dynamics of the number of patients with diseases of the esophagus and the general time trend.

Type 2 diabetes mellitus characterized by chronic hyperglycaemia is caused by insulin resistance and β-cell dysfunction. Glycogen accumulation, due to impaired metabolism, contributes to this "glucotoxicity" via dysregulated biochemical pathways promoting β-cell dysfunction. Thus, long-term exposition of insulin-secreted cells or isolated islets together with increased free fatty acids (FFA) and glucose levels can cause insulin-induced glucose secretion depression, damage to insulin gene expression and apoptotic death of cells. It is known that, the main regulator of pancreatic β-cells functioning and regulator of insulin gene expression, synthesis and secretion of insulin is glucose. Glucose enters cells and progressively metabolizes, in particular, to pyruvate in a cycle of tricarboxylic acids, subjected to oxidative phosphorylation, during which formed adenosine triphosphate and reactive oxygen radicals (ROS). Although, when more glucose enters the cell, there are other ways in which extra glucose can be transferred to reserve and of the glucose molecules can form ROS. The release of excessive amounts of FFA leads to lipotoxicity, as lipids and metabolites produce ROS in the endoplasmic reticulum and mitochondria. This affects both adipose and non-fat tissue, making up its pathophysiology in many organs. This overview demonstrates that the insulin gene is expressed in pancreatic β-cells. Glucose is the main physiological regulator of insulin gene expression. It controls the effect of transcription factors, insulin mRNA stability, and transcription rate. Glucolipotoxicity mechanisms affect the transcription factors MafA and PDX-1. Important is the β-cells damaging, which is connected with the oxidative stress and the synthesis of ceramides.

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