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首页> 外文期刊>Journal of Cellular Physiology >Glucose and Inflammatory Cells Decrease Adiponectin in Epicardial Adipose Tissue Cells: Paracrine Consequences on Vascular Endothelium
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Glucose and Inflammatory Cells Decrease Adiponectin in Epicardial Adipose Tissue Cells: Paracrine Consequences on Vascular Endothelium

机译：葡萄糖和炎症细胞减少脂联素在心外膜脂肪组织细胞:旁分泌影响血管内皮

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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 295mg/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. (c) 2015 Wiley Periodicals, Inc.
机译：心外膜脂肪组织(吃)的来源能量表达了的心insulin-sensitizer、抗炎和抗蛋白质,脂联素。冠状动脉疾病,脂联素的生产下降。监管由葡萄糖和炎症在基质从吃和皮下脂肪组织细胞(坐)及其对内皮细胞旁分泌作用细胞。接受心脏手术的患者。脂肪生成诱导在117、200、或295 mg / dl葡萄糖,有或没有macrophage-conditioned介质(MCM)。分析了胰岛素受体实时PCR。细胞在培养与决心内皮细胞,通过揭露他们高葡萄糖和/或罗马数字,此外,从患者leukocyte-conditioned介质心肌梗塞。决心通过分析血管粘连分子的表达。u型葡萄糖的剂量反应曲线脂联素在吃,而不是坐在基质细胞。相反,罗马数字减少了adipogenesis-induced脂联素的表达吃基质细胞。吃基质增加了内皮细胞的炎症分子。强调在存在有害的影响炎症cell-conditioned介质心肌梗死患者。葡萄糖和炎症细胞减少adipogenesis-induced脂联素的表达吃的基质细胞,诱导炎症在内皮细胞旁分泌过程。炎症效应是低的成熟的脂肪细胞,脂联素的生产商。这些结果有助于理解吃障碍冠状动脉的作用动脉粥样硬化进展。231: 1015 - 1023, 2016。公司。

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