Adipose tissue inflammation possibly linked to vascular injury and increased cardiovascular risk in obese subjects
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In experimental studies, adipose tissue inflammation appears etiologically linked to obesity-induced systemic inflammation, with many dysregulated adipocytokines actually originating from non-adipocytic cells, e.g. fat tissue macrophages. This study aimed to characterize the state of inflammation in human fat in relation to vascular function and metabolic parameters. To this end, subcutaneous abdominal fat was collected in 77 obese subjects, adipose macrophage population was quantified using targeted immunohistochemistry, and brachial artery vasodilator function was assessed using high-resolution vascular ultrasound. Compared to subjects with quiescent noninflamed adipose architecture, an inflamed adipose phenotype (n = 50 subjects), characterized by tissue macrophage accumulation in crown-like structures, was associated with systemic hyperinsulinaemia and insulin resistance (HOMA-IR) and impaired endothelium-dependent flow-mediated vasodilatation. In addition to increased plasma hs-CRP, macrophage retention in fat was linked to upregulated tissue CD68 and tumor necrosis factor (TNF)-alpha mRNA expression. In conclusion, in this cohort study of obese subjects, proinflammatory changes in adipose tissue were associated with systemic arterial dysfunction and insulin resistance. Adipose tissue inflammation might be linked to vascular injury and increased cardiovascular risk in obese subjects.
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