The mechanisms of oxidative stress in adipocytes of local fat depots in patients with cardiometabolic diseases have been studied insufficiently.Purpose. To study the levels of reactive oxygen species (ROS) production in adipocytes of epicardial (EAT) and subcutaneous adipose tissue (SAT) in patients with stable coronary artery disease (CAD) and severe coronary atherosclerosis who underwent coronary artery bypass grafting; to investigate the potential relationships between the levels of ROS production by EAT and SAT adipocytes and obesity parameters, EAT accumulation, basal and postprandial glycemia, and blood lipid transport function.Material and Methods. The study included 19 patients (12 men and 7 women including 6 patients (31.5%) with type 2 diabetes mellitus) aged 53–72 years with stable CAD and severe coronary atherosclerosis. The material for the study was EAT and SAT adipocytes obtained by the enzymatic method from intraoperative explants. The ROS level in adipocytes was determined using the fluorimetry with 2,3-dihydrodichlorofluorescein diacetate. Anthropometric parameters of obesity and EAT thickness were studied using echocardiography. The blood lipid transport function and the levels of basal and postprandial glucose were assessed.Results. The levels of ROS production by EAT and SAT adipocytes in the overall group of patients did not differ significantly and amounted to 1710 (1608; 2079) and 1876 (1374; 2215) arbitrary units, respectively. The level of ROS production by SAT adipocytes did not correlate with the parameters of obesity, EAT thickness, or biomarker levels. The level of ROS production by EAT adipocytes directly correlated with the level of postprandial glycemia (rs = 0.62, p < 0.05), but did not correlate with measures of general and abdominal obesity, EAT thickness, and dyslipidemia. The level of ROS production by EAT adipocytes in patients with postprandial glycemia ≥ 7.7 mmol/L (n = 9) exceeded the corresponding value in patients with lower level of postprandial glycemia (n = 10): 2079 (1710; 2458) against 1625.5 (1332; 1699) arbitrary units (p = 0.015), respectively.Conclusion. We showed for the first time that the level of ROS production by EAT adipocytes in CAD patients with severe coronary atherosclerosis was directly associated with the level of postprandial glycemia. The highest level of ROS production in EAT adipocytes occurred in these patients when the level of postprandial glycemia exceeds 7.7 mmol/L.
It has been well established that opioid peptides (OPs) affect various hormonal systems. Opioids exhibit stress-limiting and gastro-protective effects in stressed animals, acting via μ- and δ-opioid receptors (OR). Peripheral μ-OR stimulation by endogenous and exogenous opioids increases cardiac tolerance to pathological consequences of stress. Enhancement of prostacyclin synthesis, decrease of thromboxane production as well as suppression of lipid peroxidation can be directly responsible for cardioprotective effects of OPs in stressed animals. Adaptive responses are accompanied by increased OP levels in blood and tissues. Reduction of ventricular arrhythmias induced by repeated short-term immobilization stress is mediated via μ-OR stimulation by endogenous opioids, while δ-OR account for an antiarrhythmic effect of adaptation to chronic intermittent hypobaric hypoxia. The mechanism of infarct size-limiting effect of continuous normobaric hypoxia involves both μ- and δ-OR stimulation. Peptide OR agonists can be considered in future clinical practice for treatment of withdrawal syndrome, stress-related cardiac disease or myocardial injury caused by ischemia-reperfusion insult.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.