Leptin and its receptors have been identified as key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity and metabolic disorders, such as insulin resistance and dyslipidemia. Mechanisms underlying the development of leptin resistance include mutations in the genes encoding leptin and its receptors, as well as proteins involved in self-regulation of leptin synthesis and blood–brain barrier permeability. Leptin resistance encompasses a complex pathophysiological phenomenon with a number of potential research lines. In this review, we analyze the existing data on the methods used to diagnose leptin resistance.

Despite the existing preventative and therapeutic measures, cardiovascular diseases remain the main cause of temporary disability, long-term disability, and mortality. Obesity is a major risk factor for cardiovascular diseases and their complications. However, not all fat depots have the same inflammatory, paracrine, and metabolic activities. In addition, recent studies have indicated that the accumulation of visceral fat, rather than subcutaneous fat, is associated with increased cardiometabolic risk. However, there is also evidence that increasing the area of visceral fat can help protect against lipotoxicity. This review aims to discuss the contemporary literature regarding the characteristics of the visceral, epicardial, and perivascular fat depots, as well as their associations with cardiovascular disease.

Determination of the impact of visceral obesity and epicardial adipose tissue thickness on stimulating growth factor levels during hospitalization for myocardial infarction is of potential importance for predicting outcomes and assessing the development of cardiofibrotic changes associated with maladaptive myocardial remodeling. In this study, we aimed to investigate the relationships between epicardial adipose tissue thickness, adipokine profiles, and the stimulating growth factor 2/interleukin-33 signaling system during hospitalization for myocardial infarction, and with the cardiac fibrosis extent 1-year post-MI in patients with visceral obesity. Eighty-eight patients with myocardial infarction were grouped based on their visceral obesity. Serum leptin, adiponectin, stimulating growth factor 2, and interleukin-33 levels were measured on days 1 and 12 and at 1 year. The epicardial adipose tissue widths and the cardiac fibrosis areas were measured on day 12 and at 1 year. Visceral obesity was associated with epicardial adipose tissue thickness increases, adipokine imbalances, elevated leptin levels, and lower adiponectin levels during early hospitalization, and cardiac fibrosis development. Patients without visceral obesity had higher interleukin-33 and stimulating growth factor 2 levels during early hospitalization and lower cardiac fibrosis rates. Epicardial adipose tissue thickness was positively associated with cardiac fibrosis prevalence and interleukin-33 levels and negatively associated with stimulating growth factor 2 levels. The cardiac fibrosis extent was negatively associated with interleukin-33 levels and positively associated with stimulating growth factor 2 levels. Increases in epicardial adipose tissue thickness are associated with cardiac fibrosis development 1-year post-myocardial infarction and are higher in patients with visceral obesity. The metabolic activity of the epicardial adipose tissue is associated with elevated interleukin-33 and reduced stimulating growth factor 2 levels.

Adipose tissue (AT) is an endocrine and paracrine organ that synthesizes biologically active adipocytokines, which affect inflammation, fibrosis, and atherogenesis. Epicardial and perivascular fat depots are of great interest to researchers, owing to their potential effects on the myocardium and blood vessels. The aim of the study was to assess the expression and secretion of adipocytokine genes in the AT of patients with coronary artery disease (CAD) and patients with aortic or mitral valve replacement. This study included 84 patients with CAD and 50 patients with aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous, epicardial (EAT), and perivascular AT (PVAT), and were cultured for 24 h. EAT exhibited the lowest level of adiponectin gene expression and secretion, regardless of nosology, and high expression levels of the leptin gene and interleukin-6 (IL-6). However, EAT adipocytes in patients with CAD were characterized by more pronounced changes in comparison with the group with heart defects. High leptin and IL-6 levels resulted in increased pro-inflammatory activity, as observed in both EAT and PVAT adipocytes, especially in individuals with CAD. Therefore, our results revealed the pathogenetic significance of alterations in the adipokine and cytokine status of adipocytes of EAT and PVAT in patients with CAD.

Free fatty acids (FFA), oxidized low-density lipoprotein (LDL) and its antibodies, lipid profile markers, which are formed under oxidative stress, play an important role in atherosclerotic disease. Assess the levels of these markers in myocardial infarction patients depending on the extent of coronary artery disease (CAD). ST-elevation MI patients with hemodynamically significant stenoses of ≥75% in one, two, three, or more coronary arteries were examined. The patients were divided into three groups according to the severity of coronary lesions. Patients had a ≥75% stenotic lesion in one coronary artery (group 1, n = 135), two coronary arteries (group 2, n = 115), or three or more coronary arteries (group 3, n = 150). The control group comprised healthy subjects (n = 33). FFA levels on day 1 from MI onset were higher in groups 1, 2, and 3 compared with controls. On day 1 from MI onset, oxidized LDL levels were significantly higher in groups 2 and 3 than those in controls (both р = 0.001). Oxidized LDL levels were significantly higher in patients with multivessel CAD compared with those with single-vessel CAD on days 1 and 12. Antibody levels increased with the number of affected arteries. High levels FFA, oxidized LDL and its antibody, lipid profile markers, and parameters of the pro/antioxidant systems persist during the subacute phase of MI.

Background: Insulin resistance (IR) is a risk factor for ischaemic heart disease and myocardial infarction (MI). IR often manifests in MI and is regarded as an independent predictor of in-hospital mortality, which can provide early risk stratification for recurrent acute coronary events. Methods: The study enrolled 200 patients (130 males and 70 females aged 61.4 ± 1.12 years) diagnosed with ST elevation MI. At days 1 and 12 from the MI onset, IR levels and lipid profiles, as well as serum glucose, insulin, adipokine and ghrelin levels, were measured. Results: Free fatty acid (FFA) levels had the most pronounced changes: IR patients had a 9-fold increase in FFA levels at day 1, and patients without IR had a 6-fold increase. Leptin levels at days 1 and 12, in IR patients were, on average, 1.5- and 2-fold higher compared to the controls and patients with no IR (р < 0.05). Leptin levels in IR patients were increased throughout the entire hospital stay. Resistin levels in IR patients were, on average, 1.4-fold higher throughout the entire hospital stay, while in non-IR patients, resistin levels were similar to the controls. Adiponectin levels in IR patients were decreased compared to the controls, while in patients with IR, they were similar to the controls. Both IR and non-IR MI patients had 3-fold and 3.7-fold lower ghrelin levels at day 1, respectively, compared to the controls. The correlation analysis showed a negative correlation between ghrelin and FFA (r = −0.48 р = 0.007), ghrelin and leptin (r = −0.4 р = 0.003), ghrelin and insulin (r = −0.54 р = 0.002), and ghrelin and glucose (r = −0.31 р = 0.002) in MI patients. Conclusion: Dyslipidaemia, along with insulinaemia and glycaemia, is one of the most significant IR risk factors in the acute and early recovery phases of MI. Dyslipidaemia is characterised by a high FFA level; an imbalance of leptin, resistin, and adiponectin; and a deficiency of ghrelin in the acute and early recovery periods of MI. FFA and ghrelin can be used as promising molecular markers to stratify the risk of recurrent acute coronary events and diabetes mellitus in MI patients.