SFEBES2007 Oral Communications British Thyroid Association Award (5 abstracts)
Comparsion of the NFκB and JNK mediated inflammatory mechanisms for production of adipocytokines in paired human epicardial and gluteo-femoral adipose tissue from CABG patients
Adam R Baker 1 , Alison L Harte 1 , Nancy F da Silva 1 , Margaret J Hill 1 , Aaron Ranasinghe 2 , Kamlesh Khunti 3 , Melanie J Davies 4 , Dominico Pagano 2 , Robert Bonser 2 , Sudhesh Kumar 1 & Philip G McTernan 1
1University of Warwick, Unit for Diabetes & Metabolism, Coventry, United Kingdom; 2University of Birmingham, Dept. of Cardiothoracic Surgery, Birmingham, United Kingdom; 3University of Leicester, Division of General Practice, Leicester, United Kingdom; 4University Hospitals of Leicester, Diabetes Research Unit, Leicester, United Kingdom.
Adipose tissue (AT) distribution impacts directly on type 2 diabetes and cardiovascular disease risk, however few studies have investigated the site-specific nature of human epicardial AT compared with gluteo-femoral (thigh) fat. Our recent studies have implicated epicardial AT as an important source of pro-inflammatory cytokines which may impact on myocardial function. Therefore the aim of this study was, using matched paired epicardial AT and gluteo-femoral (thigh) AT from patients undergoing coronary artery bypass grafting (CABG), to examine (1) the key mediators of the innate immune pathway toll like receptors, TLR 2 and TLR 4, and NFκB and c-jun kinase (JNK), also mediators of adipocytokine production (2) macrophages in epicardial adipose tissue (3) and whether circulating endotoxin may represent a potential mediator for immune activation. Fasted serum was taken from CABG (Age:63.8±8.4 yrs, BMI:27.8±3.5 kg/m2, n=72) and Non-CAD subjects (Age:61.8±8.0 yrs, BMI:27.9±3.3 kg/m2, n=60). Paired epicardial and thigh AT was obtained from CABG subjects (n=16). mRNA data in epicardial AT showed strong correlations between CD-68 (marker of macrophages) with TLR-2 (r=0.94, P<0.001), TLR-4 (r=0.95, P<0.001) and TNFα (r=0.81, P<0.001). Protein expression data showed epicardial AT had significantly higher NFκB, IKK-γ, IKK-β and JNK compared with thigh AT (NFκB, P=0.06; IKKβ, P=0.01; IKKγ, P=0.001; JNK P<0.01; n=4). Finally, circulating endotxin was raised in CABG patients compared with age and BMI matched controls (CABG: 5.52±0.57 EU/mL vs Controls: 6.80±0.28 EU/mL, P=0.047). In summary epicardial AT has increased NFκB, IKKβ and JNK expression compared with matched thigh tissue suggesting a depot specific response to inflammation in AT. Such inflammation may arise due to gut derived endotoxin activating macrophages in conjunction with the adipocytes. In conclusion, these studies highlight epicardial AT as a source of inflammatory cytokines mediated through NFκB and components of key inflammatory pathways and further highlights the role of the macrophage in inflammation within this tissue.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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