Dapagliflozin increased glucose uptake, reduced the secretion of pro-inflammatory chemokines (with a beneficial effect on the healing of human coronary artery endothelial cells), and improved the differentiation of EAT cells. These results suggest a new protective pathway for this drug on EAT from patients with cardiovascular disease.
Salgado-Somoza A, Teijeira-Fernández E, Fernández AL, González-Juanatey JR, Eiras S. Proteomic analysis of epicardial and subcutaneous adipose tissue reveals differences in proteins involved in oxidative stress. Am J Physiol Heart Circ Physiol 299: H202-H209, 2010. First published April 30, 2010; doi:10.1152/ajpheart.00120.2010.-Epicardial adipose tissue (EAT) is an endocrine organ adjacent to coronary arteries and myocardium without anatomy barriers. Locally produced adipokines may reflect or affect to cardiovascular physiology and pathology. Our aim was to study the protein expression profiles of EAT and subcutaneous adipose tissue (SAT) to identify local candidate molecules characterizing EAT in patients with cardiovascular disease. EAT and SAT samples were collected from 55 patients undergoing heart surgery. Proteins from these tissues were separated by two-dimensional (2D) gel electrophoresis, and differences between them were identified by MALDI-TOF/TOF spectra. Differences in protein levels were further investigated by real-time RT-PCR and Western blots, and production of reactive oxygen species (ROS) in EAT and SAT was evaluated by nitroblue tetrazolium chloride assays. ROS production was higher in EAT than SAT. We have found mRNA differences for catalase, glutathione S-transferase P, and protein disulfide isomerase, and 2D Western blots additionally showed post-translational differences for phosphoglycerate mutase 1; all four are related to oxidative stress pathways. EAT suffers greater oxidative stress than SAT in patients with cardiovascular diseases and exhibits associated proteomic differences that suggest the possibility of its association with myocardial stress in these patients. epicardial adipose tisssue OBESITY IS ONE OF THE MAIN causes of metabolic diseases. It is associated with a chronic inflammatory response and cardiovascular diseases (34). However, risk depends significantly on the distribution of adipose tissue in the body; for example, metabolic risk factors were more associated with omental adipose tissue (OAT) than with subcutaneous adipose tissue (SAT) among 3,001 participants in the Framingham Heart Study (6). These differences are plausibly due to different adipose tissues differing in adipokine expression and the production of inflammatory reactive oxygen species (ROS), which are known to be associated with cardiovascular disease (8); OAT is associated with more circulating substances related to inflammation and oxidative stress than SAT is (24).Epicardial adipose tissue (EAT) is a visceral fat pad adjacent to coronary arteries and the myocardium (11). The amount of EAT is related to left ventricle mass (13) and to the amount of intra-abdominal visceral fat, and visceral adiposity can in fact be evaluated by means of its echocardiographic measurement (10). Like other adipose tissues, EAT is now recognized as an endocrine organ, and its proximity to myocardium and coronary arteries suggests the possibility of paracrine action on these structures. In fact, in patients with coronary ...
Low plasma adiponectin levels are related to a higher risk of development of metabolic and cardiovascular disorders, including hypertension (HT). To date, there have been no studies supporting the relationship between epicardial adipose tissue (EAT) expression of adiponectin and HT. We collected samples of EAT from 116 patients undergoing elective cardiac surgery, mostly for coronary artery bypass grafting (n ¼ 54), valve surgery (n ¼ 49) or both (n ¼ 12). Samples of subcutaneous adipose tissue (SAT) were harvested from 85 patients. After RNA isolation, the expression of adiponectin was analysed by real-time retrotranscriptase (RT)-PCR. Baseline clinical data were obtained from medical records. The diagnosis of HT was established mostly by the patients' general physicians following current guidelines. We included 84 hypertensive and 32 non-hypertensive patients. Mean ( ± s.d.) age was 70.3±7.9 years. EAT expression levels of adiponectin were lower in hypertensives (14.0 ± 3.6 vs 15.3 ± 3.6 arbitrary units (a.u.), P ¼ 0.06). This difference was statistically significant (odds ratio (OR) 0.828 per a.u., P ¼ 0.020) after adjustment for age, gender, body mass index, diabetes mellitus, heart failure, coronary artery disease (CAD), total cholesterol and triglyceride levels. However, SAT adiponectin mRNA levels were similar in hypertensive and non-hypertensive patients (15.3 ± 4.2 vs 15.3 ± 5.0 a.u., P40.99). Adjustment for potential confounding factors hardly altered this result. Our findings indicate that EAT expression of adiponectin may be associated with HT status independently of CAD or other comorbidities, whereas SAT expression does not. These results support the hypothesis that EAT is actively implicated in global cardiovascular risk, describing its association with HT.
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