Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and its Complications (HNDC), Athens, Greece.
Cardiovasc Diabetol. 2011 Feb 1;10:14. doi: 10.1186/1475-2840-10-14.
Adiponectin has insulin-sensitizing and anti-atherosclerotic effects, partly mediated through its action on monocytes. We aimed to determine adiponectin levels and expression of its receptors (AdipoR1 and AdipoR2) in peripheral monocytes from overweight and obese patients with coronary artery disease (CAD).
Fifty-five overweight/obese patients, suspected for CAD, underwent coronary angiography: 31 were classified as CAD patients (stenosis ≥ 50% in at least one main vessel) and 24 as nonCAD. Quantitative RT-PCR and flow cytometry were used for determining mRNA and protein surface expression of adiponectin receptors in peripheral monocytes. A high sensitivity multiplex assay (xMAP technology) was used for the determination of plasma adiponectin and interleukin-10 (IL-10) secreted levels.
Plasma adiponectin levels were decreased in CAD compared to nonCAD patients (10.9 ± 3.1 vs. 13.8 ± 5.8 μg/ml respectively, p = 0.033). In multivariable analysis, Matsuda index was the sole independent determinant of adiponectin levels. AdipoR1 and AdipoR2 protein levels were decreased in monocytes from CAD compared to nonCAD patients (59.5 ± 24.9 vs. 80 ± 46 and 70.7 ± 39 vs. 95.6 ± 47.8 Mean Fluorescence Intensity Arbitrary Units respectively, p < 0.05). No significant differences were observed concerning the mRNA levels of the adiponectin receptors between CAD and nonCAD patients. AdipoR2 protein levels were positively correlated with plasma adiponectin and Matsuda index (r = 0.36 and 0.31 respectively, p < 0.05 for both). Furthermore, basal as well as adiponectin-induced IL-10 release was reduced in monocyte-derived macrophages from CAD compared to nonCAD subjects.
Overweight patients with CAD compared to those without CAD, had decreased plasma adiponectin levels, as well as decreased surface expression of adiponectin receptors in peripheral monocytes. This fact together with the reduced adiponectin-induced IL-10 secretion from CAD macrophages could explain to a certain extent, an impaired atheroprotective action of adiponectin.
脂联素具有胰岛素增敏和抗动脉粥样硬化作用，部分通过其对单核细胞的作用介导。我们旨在确定超重和肥胖的冠心病（CAD）患者外周血单核细胞中的脂联素水平及其受体（AdipoR1 和 AdipoR2）的表达。
55 名超重/肥胖疑似 CAD 的患者接受冠状动脉造影：31 名患者被归类为 CAD 患者（至少一条主要血管狭窄≥50%），24 名患者为非 CAD 患者。使用定量 RT-PCR 和流式细胞术检测外周血单核细胞中脂联素受体的 mRNA 和蛋白表面表达。使用高灵敏度多重分析（xMAP 技术）测定血浆脂联素和白细胞介素-10（IL-10）的分泌水平。
与非 CAD 患者相比，CAD 患者的血浆脂联素水平降低（分别为 10.9±3.1 和 13.8±5.8μg/ml，p=0.033）。多元分析显示，Matsuda 指数是脂联素水平的唯一独立决定因素。与非 CAD 患者相比，CAD 患者的单核细胞中 AdipoR1 和 AdipoR2 蛋白水平降低（分别为 59.5±24.9 和 70.7±39 与 80±46 和 95.6±47.8 Mean Fluorescence Intensity Arbitrary Units，p<0.05）。CAD 和非 CAD 患者之间，脂联素受体的 mRNA 水平无显著差异。AdipoR2 蛋白水平与血浆脂联素和 Matsuda 指数呈正相关（r=0.36 和 0.31，p<0.05）。此外，与非 CAD 患者相比，CAD 患者的单核细胞衍生巨噬细胞中，基础和脂联素诱导的 IL-10 释放减少。
与无 CAD 的患者相比，超重的 CAD 患者的血浆脂联素水平降低，外周血单核细胞中脂联素受体的表面表达也降低。这一事实以及 CAD 巨噬细胞中脂联素诱导的 IL-10 分泌减少，在一定程度上可以解释脂联素的抗动脉粥样硬化作用受损。
