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Glucose and Inflammatory Cells Decrease Adiponectin in Epicardial Adipose Tissue Cells: Paracrine Consequences on Vascular Endothelium

Epicardial adipose tissue (EAT) is a source of energy for heart that expresses the insulin‐sensitizer, anti‐inflammatory and anti‐atherogenic protein, adiponectin. But, in coronary artery disease, adiponectin production declines. Our objective was to determine its regulation by glucose and inflammation in stromal cells from EAT and subcutaneous adipose tissue (SAT) and its paracrine effect on endothelial cells. Stromal cells of EAT and SAT were obtained from patients who underwent cardiac surgery. Adipogenesis was induced at 117, 200, or 295 mg/dl glucose, with or without macrophage‐conditioned medium (MCM). Expression of adiponectin, GLUT‐4 and the insulin receptor was analyzed by real‐time PCR. The paracrine effect of stromal cells was determined in co‐cultures with endothelial cells, by exposing them to high glucose and/or MCM, and, additionally, to leukocyte‐conditioned medium from patients with myocardial infarction. The endothelial response was determined by analyzing vascular adhesion molecule expression. Our results showed a U‐shaped dose–response curve of glucose on adiponectin in EAT, but not in SAT stromal cells. Conversely, MCM reduced the adipogenesis‐induced adiponectin expression of EAT stromal cells. The presence of EAT stromal increased the inflammatory molecules of endothelial cells. This deleterious effect was emphasized in the presence of inflammatory cell‐conditioned medium from patients with myocardial infarction. Thus, high glucose and inflammatory cells reduced adipogenesis‐induced adiponectin expression of EAT stromal cells, which induced an inflammatory paracrine process in endothelial cells. This inflammatory effect was lower in presence of mature adipocytes, producers of adiponectin. These results contribute to understanding the role of EAT dysfunction on coronary atherosclerosis progression. J. Cell. Physiol. 231: 1015–1023, 2016. © 2015 Wiley Periodicals, Inc.