Relationship between monocyte/macrophage activation marker soluble CD163 and insulin resistance in obese and normal-weight subjects.

Relationship between monocyte/macrophage activation marker soluble CD163 and insulin resistance in obese and normal-weight subjects.
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DOI:
10.1111/j.1365-2265.2011.04284.x
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发表时间:
2012-09
影响因子:
3.2
通讯作者:
Grinspoon SK
Grinspoon SK
中科院分区:
医学3区
文献类型:
--
作者:
Zanni MV;Burdo TH;Makimura H;Williams KC;Grinspoon SK

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单核细胞/巨噬细胞活化与肥胖症胰岛素抵抗的关系尚不清楚。研究巨噬细胞活化标志物可溶性CD 163(sCD 163)与肥胖和正常体重受试者胰岛素抵抗和代谢参数的关系。研究了95名健康受试者(65名肥胖和30名正常体重)。血浆中的sCD 163浓度进行了评估,以及葡萄糖稳态,人体测量学,细胞因子和脂肪因子的标志物。研究sCD 163与这些参数之间的关系,并进行多元回归模型评估sCD 163对胰岛素抵抗(HOMA-IR)的贡献。与正常体重对照组相比,肥胖受试者的sCD 163显著升高[974(657,1272)ng/ml vs. 599(423,892)ng/ml,中位数(IQR); p < 0.0001]。sCD 163与HOMA-IR(斯皮尔曼rho = 0.37,p = 0.0003)和其他代谢参数密切相关。在log HOMA-IR的多元回归模型中,sCD 163仍然显著相关(p = 0.005),控制了已知的胰岛素抵抗介质,包括年龄、性别、内脏肥胖和炎症标志物(模型R2 = 0.54,p < 0.0001)。对log HOMA-IR的其他嵌套多元回归模型显示,sCD 163比其他脂肪因子和炎症标志物更能预测HOMA-IR。在控制了已知的胰岛素抵抗介质后,正常体重和肥胖受试者中,单核细胞/巨噬细胞活化(如sCD 163水平所反映)与HOMA-IR密切相关。此外,sCD 163增加了预测胰岛素抵抗的标准风险标志物。这些数据表明,单核细胞/巨噬细胞活化可能是肥胖胰岛素抵抗的重要决定因素。
The relationship of monocyte/macrophage activation to insulin resistance in obesity is unknown. To investigate a marker of macrophage activation, soluble CD163 (sCD163), in relationship to insulin resistance and metabolic parameters in obese and normal-weight subjects. 95 healthy subjects (65 obese and 30 normal-weight) were studied. Plasma concentrations of sCD163 were assessed, as well as markers of glucose homeostasis, anthropometrics, cytokines, and adipokines. The relationships between sCD163 and these parameters were investigated, and multiple regression modeling assessing the contribution of sCD163 to insulin resistance (HOMA-IR) was performed. sCD163 was significantly increased in obese subjects compared to normal-weight controls [974 (657, 1272) ng/ml vs. 599 (423, 892) ng/ml, median (IQR); p < 0.0001]. sCD163 was strongly associated with HOMA-IR (Spearman's rho = 0.37, p = 0.0003) and other metabolic parameters. In multiple regression modeling for log HOMA-IR, sCD163 remained significantly associated (p = 0.005) controlling for known mediators of insulin resistance including age, gender, visceral adiposity, and inflammatory markers (model R2 = 0.54, p < 0.0001). Additional nested multiple regression models for log HOMA-IR showed that sCD163 added more than other adipokines and inflammatory markers to the prediction of HOMA-IR. Monocyte/macrophage activation, as reflected by sCD163 levels, is strongly associated with HOMA-IR in normal-weight and obese subjects after controlling for known mediators of insulin resistance. Moreover, sCD163 adds to standard risk markers for predicting insulin resistance. These data suggest that monocyte/macrophage activation may be an important determinant of insulin resistance in obesity.
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