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• W2013543828 abstract "Objective . Adipose tissue (AT) macrophages are increased in obesity and associated with low grade inflammation. We aimed to characterize the phenotype of AT macrophages in humans in relation to obesity and insulin resistance. Design . Gene-expression levels of general macrophage markers (CD68 and CD14), proinflammatory markers/M1 (TNF- α , MCP-1, and IL-6), and anti-inflammatory markers/M2 (CD163, CD206, and IL-10) were determined by RT-PCR in subcutaneous AT samples from lean and obese subjects. Insulin resistance was determined by HOMA-IR. Results . All the macrophage markers were elevated in the AT from obese compared to lean subjects (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mi>P</mml:mi><mml:mo><</mml:mo><mml:mn>0.001</mml:mn></mml:math>). To determine the phenotype of the macrophages the level of CD14 was used to adjust the total number of macrophages. The relative expression of CD163 and IL-10 was elevated, and TNF- α and IL-6 were reduced in AT from obese subjects (all<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mi>P</mml:mi><mml:mo><</mml:mo><mml:mn>0.05</mml:mn></mml:math>). In a multivariate regression analysis CD163 was the only macrophage marker significantly associated with HOMA-IR ( β : 0.57;<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M3><mml:mi>P</mml:mi><mml:mo><</mml:mo><mml:mn>0.05</mml:mn></mml:math>). Conclusion. Obesity is associated with elevated numbers of macrophages in the AT. Unexpectedly, the macrophages change phenotype by obesity, with a preponderance of M2 and a decrement of M1 markers in AT from obese subjects. Moreover, CD163 was the only macrophage marker associated with HOMA-IR after multiple adjustments." @default.
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• W2013543828 date "2014-01-01" @default.
• W2013543828 modified "2023-10-15" @default.
• W2013543828 title "Human Adipose Tissue Macrophages Are Enhanced but Changed to an Anti-Inflammatory Profile in Obesity" @default.
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• W2013543828 doi "https://doi.org/10.1155/2014/309548" @default.
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