Adiponectin is thought to play a decisive role in the relationships among obesity, insulin resistance and cardiovascular risk. This study investigated whether cardiomyocytes synthesize and secrete adiponectin, and the effects of this hormone on cardiac cells. RT-PCR showed that mouse, rat and human cardiomyocytes produced mRNA for adiponectin and adiponectin receptors 1 and 2. Immunohistochemistry confirmed the presence of adiponectin in the cytoplasm of cultured cardiomyocytes, and radioimmunoassay showed that these cells secreted adiponectin into the culture medium. Exogenous adiponectin enhanced glucose and fatty acid uptake and induced AMPK phosphorylation in cultured cardiomyocytes. Our results demonstrate that adiponectin is synthesized and secreted by isolated murine and human cardiomyocytes, and suggest that the local production of this hormone by cardiomyocytes could be involved in the regulation of cardiac metabolism and function.

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 ...

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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.

Changes in myosin heavy chain (MHC) isoform expression and protein composition occur during cardiac disease and it has been suggested that even a minor shift in MHC composition may exert a considerable effect on myocardial energetics and performance. Here an overview is provided of the cellular basis of the energy utilisation in cardiac tissue and novel data are presented concerning the economy of myocardial contraction in diseased atrial and ventricular human myocardium. ATP utilisation and force development were measured at various Ca(2+) concentrations during isometric contraction in chemically skinned atrial trabeculae from patients in sinus rhythm (SR) or with chronic atrial fibrillation (AF) and in ventricular muscle strips from non-failing donor or end-stage failing hearts. Contractile protein composition was analysed by one-dimensional gel electrophoresis. Atrial fibrillation was accompanied by a significant shift from the fast alpha-MHC isoform to the slow beta-MHC isoform, whereas both donor and failing ventricular tissue contained almost exclusively the beta-MHC isoform. Simultaneous measurements of force and ATP utilisation indicated that economy of contraction is preserved in atrial fibrillation and in end-stage human heart failure.

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