Key result
Patients with coronary artery disease had lower peripheral plasma adiponectin concentrations compared to non-CAD controls.
Why the study?
Is adiponectin expression in epicardial adipose tissue altered in patients with coronary artery disease?
Observational (n=34)
No
Is adiponectin expression in epicardial adipose tissue altered in patients with coronary artery disease?
Decreased adiponectin in epicardial adipose tissue is associated with increased inflammation in CAD patients, suggesting a protective role against macrophage-mediated inflammation.
Answers are grounded in this paper and cite their sources.
Lower adiponectin in CAD patients may reflect heightened inflammation; leaves open whether epicardial modulation offers therapeutic targets.
BACKGROUND: Disorders of endocrine substances in epicardial adipose tissue are known causes of coronary artery disease (CAD). Adiponectin is associated with cardiovascular disease. However, expression of adiponectin in epicardial adipose tissue and its function in CAD pathogenesis is unclear. This study investigates adiponectin expression in epicardial adipose tissue in CAD patients. METHODS: Vessels or adipose tissue samples collected from CAD patients and non-CAD controls were examined after immunochemical staining. Adiponectin, cytokines of interleukin-6 (IL-6) and necrosis factor-α (TNF-α) and toll-like receptor 4 (TLR4) expression level in adipose tissue were measured using real-time quantitative RT-PCR. Adiponectin concentrations in peripheral and coronary sinus vein plasma were measured with enzyme-linked immunosorbent assay. Peripheral vein plasma biochemistries were performed with routine laboratory techniques. Monocytes were collected from blood using lymphocyte separation medium. Expression level of cytokines and transcription factor NF-κB were measured to learn the effect of adiponectin on stearic acid-stimulated monocytes. Percentage of TLR4 positive monocytes was analyzed using flow cytometry. RESULTS: Histological examination revealed increased macrophage infiltration into epicardial adipose tissue of CAD patients. Decreased adiponectin displayed by real-time quantitative RT-PCR was associated with enhanced cytokines of IL-6 and TNF-α or TLR4 expression level in epicardial adipose tissue, suggesting decreased circulating adiponectin may be useful as a more sensitive predictor for coronary atherosclerosis than routine laboratory examinations. Adiponectin suppressed secretion of IL-6 and TNF-α in stimulated monocytes and TLR4 was expressed on cell surfaces. CONCLUSIONS: Endocrine disorders in epicardial adipose tissue are strongly linked to CAD, and adiponectin has a protective effect by inhibiting macrophage-mediated inflammation.
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Zhou et al. (2011) conducted an observational in Coronary artery disease (n=34). Coronary artery disease vs. Non-CAD controls was evaluated on Peripheral plasma adiponectin concentration (μg/ml) (p=<0.01). Patients with coronary artery disease had lower peripheral plasma adiponectin concentrations compared to non-CAD controls.
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