Inflammation of adipose tissue. Is there a place for statins to correct adiposopathy?

This review is devoted to the analysis of data on the effect of inhibitors of 3-hydroxy-3-methylglutaryl coenzymate-reductase on the endocrine function of adipose tissue in obesity. Violation of metabolism of adipose tissue, as well as the amount of fat, are a a key factor in the pathophysiology of obesity and the development of concomitant diseases. Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl-kofermenta reductase (HMG-COA reductase) that catalyze the initial stage of cholesterol biosynthesis in the liver. Therefore, traditionally, the liver is considered as the main target organ for statins. The results of studies of molecular mechanisms of action of statins on carbohydrate and lipid metabolism, adipokine and inflammatory balance in adipose tissue on the example of isolated adipocytes (in vivo) and in living organism (in vitro) are presented. Effect of statins on the action of insulin, as well as the possibility of developing pathological conditions associated with insulin resistance and the development of type 2 diabetes mellitus (DM 2). The proven clinical effects of cholesterol-lowering action of statins, allow new insights and to further explore their possible impact on other links in the development of obesity, and potentially to use them as therapeutic agents for pharmacological correction of obesity and the fight against cardiovascular diseases

Body fat distribution: the answer to the apparent paradox of obesity in cardiology?

Today, despite all the measures taken, cardiovascular diseases remain the main cause of temporary invalidization, disability and mortality. Obesity is a major risk factor of cardiovascular diseases and complications from them. However, not all fat depots have the same proinflammatory, paracrine and metabolic activity. Recent studies have shown that the accumulation of visceral fat, and not subcutaneous fat, is associated with an increase in cardiometabolic risk. At the same time, there is evidence that an increase in the area of visceral fat is a protective mechanism against lipotoxicity. The purpose of this review is to discuss current literature data reflecting the characteristics of the visceral, epicardial and perivascular fat depots, and also their association with cardiovascular diseases

Thе role of zinc in the development of cardiovascular complications in patients with Graves’ disease

Backgraund. The development of cardiovascular complications in patients with diffuse-toxic goiter (DTZ) is an actual problem of thyroidology. (SSS) in patients with DTZ. Aims. To assess the contribution of zinc deficiency in the formation of cardiovascular complications in patients with Graves disease. Methods. The study included 113 women aged 2560 years with the diagnosis of DTZ: 54.0% (n = 61) with an average severity of thyrotoxicosis, 46.0% (n = 52) with severe. Duration of the disease is 15 years. The control group consisted of 37 women aged 2560 years without pathology of the thyroid gland and CCC. All patients were evaluated: in the blood the level of thyroid-stimulating hormone (TTG), free thyroxine (over T4), the concentration of antibodies to the thyroid-stimulating hormone receptor (AT to RTTG); in the hair the concentration of zinc; ultrasound (ultrasound) of the thyroid gland, echocardiography (EchoCG), daily monitoring of electrocardiography (CM ECG). Results. At DTZ deficiency of zinc in hair was observed in 66.4% (n = 75), in the control group in 27.0% (n = 10) patients (p = 0.01). More often, zinc deficiency was found at a severe degree of DTZ in 82.7% (n = 43), atrial fibrillation (AF) in 77.4% (n = 24) cases, in CHF 78.8% (n = 41) cases. The diagnostic model and the table of risk factors of CHF in points, including the definition of the level of zinc in the hair, are developed with the help of logistic regression. It is advisable to use the table for all patients with DTZ to determine the degree of CHF risk, with an average and high risk of developing CHF in the treatment of DTZ, it is shown to include zinc preparations. Conclusion. The obtained data allow to consider that the zinc deficiency increases the probability of development of AF and CHF in patients with DTZ of severe severity, needs diagnostics and correction

Expression of adipocytokines in heart fat depots depending on the degree of coronary artery atherosclerosis in patients with coronary artery disease.

In coronary artery disease (CAD) the adipocytokine content in the heart fat depot is altered, but it has not been established whether these changes are associated with the degree of atherosclerotic damage to the coronary artery (CA). Were examined 84 patients with CAD, and according to the degree of atherosclerotic state based on the SYNTAX Score scale, were divided: 39 moderate (≤22 points), 20 severe (23-31 points) and 25 extremely severe (≥32 points). Biopsies of subcutaneous (SAT), epicardial (EAT) and perivascular adipose tissue (PVAT) were obtained during elective coronary artery bypass grafting (CABG). The expression of adipocytokine was determined using real-time PCR. The concentration of the studied adipocytokines in adipocyte culture medium was measured by ELISA. Statistical analysis was performed using logistic regression analysis. In the adipocytes of the cardiac depot of patients with CAD, an increase in the expression and secretion of leptin and IL-6 and a decrease in adiponectin, with a maximum manifestation in severe and extremely severe CA lesions, was observed. EAT adipocytes were characterized by minimal expression of the adiponectin gene maximal gene expression leptin and IL-6 compared to SAT and PVAT adipocytes

Adipokine-cytokine profile of adipocytes of epicardial adipose tissue in ischemic heart disease complicated by visceral obesity

Introduction. To date, cardiovascular diseases (CVD) remain the main cause of disability and mortality in population. The majority of ectopic fat deposits demonstrated a reliable association with cardiometabolic risks and clinical manifestations of most CVD. The elucidation of the metabolic features of adipocytes of epicardial adipose tissue localized in the immediate vicinity of the lesion in ischemic heart disease (IHD) can have both theoretical and practical significance for pathophysiology and cardiology. Aim. To study the adipokine-cytokine profile of epicardial adipocytes (EA) and subcutaneous adipose tissue (SCAT), blood serum in relation to the area of visceral adipose tissue (AVAT), biochemical and rhelinic characteristics of IHD patients. Methods. 84 patients (70 men and 14 women) with IHD were examined. In the presence of visceral obesity (VO), patients were divided into two groups. In patients with VO, adipocyte EA and SCAT were sampled, followed by cultivation and evaluation of adipokine and proinflammatory activity. The parameters of carbohydrate and lipid metabolism, adipokine and proinflammatory status in blood serum were determined. Results. It has been established that the adipokine-cytokine profile of the adipocytes EA and SCAT differ. Adipocytes of EA in IHD on the background of VO are characterized by an increase in IL-1, TNF-α, leptin-adiponectin ratio and a decrease in the protective factors: adiponectin and anti-inflammatory cytokine IL-10. While adipocytes of SCAT were characterized by a decrease in the concentration of the soluble receptor to leptin and a more pronounced leptin resistance, and the increase in inflammatory cytokines was compensated by an increase in the concentration of IL-10, the presence of VO was associated with multivessel coronary disease, multifocal atherosclerosis, insulin resistance, atherogenic dyslipidemia, adipokine imbalance, and markers of inflammation. Thus, the value of the area of VO determined higher values of leptin concentration, TNF-α in adipocytes and serum, lipid and carbohydrate metabolism and a lower soluble receptor for leptin content. The conclusion. Thus, in IHD with VO the state of adipocytes, EA is characterized as "metabolic inflammation" and may indicate the direct involvement of adipocytes in the pathogenesis of IHD due to the formation of adipokine imbalance and the activation of proinflammatory reactions