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- Anagha Vinay Sahasrabuddhe, Shailesh U Pitale, Saravana Devi Sivanesan, Purushottam K Deshpande, Swapnil P Deshpande, and Atul Daiwile.
- Department of Physiology, NKP Salve Institute of Medical Sciences & Research Center, Nagpur, Maharashtra, India.
- Indian J Med Res. 2020 Jun 1; 151 (6): 554-561.
Background & ObjectivesCoronary artery disease (CAD), a leading cause of mortality and morbidity worldwide has multifactorial origin. Epicardial adipose tissue (EAT) has complex mechanical and thermogenic functions and paracrine actions via various cytokines released by it, which can have both pro- and anti-inflammatory actions on myocardium and adjacent coronaries. The alteration of EAT gene expression in CAD is speculated, but poorly understood. This study was undertaken to find out the difference in gene expression of epicardial fat in CAD and non-CAD patients.MethodsTwenty seven patients undergoing coronary artery bypass graft (CABG) and 16 controls (non-CAD patients undergoing valvular heart surgeries) were included in the study and their EAT samples were obtained. Gene expressions of uncoupling protein-1, monocyte chemoattractant protein-1 (MCP-1), adiponectin, adenosine A1 receptor (ADORA-1), vascular cell adhesion molecule-1 (VCAM-1) and tumour necrosis factor-alpha (TNF-α) were studied by real-time reverse transcription-polymerase chain reaction. Glucose, insulin, lipid profile, high-sensitivity C-reactive protein, homocysteine, vitamin D, TNF-α and leptin levels were estimated in fasting blood samples and analyzed.ResultsLeptin levels were significantly higher in CABG group as compared to controls (P <0.05), whereas other metabolic parameters were not significantly different between the two groups. MCP-1, VCAM-1 and TNF-α were upregulated in the CABG group as compared to controls. Further, multivariate analysis showed significantly reduced adjusted odds ratio for MCP-1 [0.27; 95% confidence interval: 0.08-0.91] in the CABG group as compared to controls (P <0.05).Interpretation & ConclusionsOur findings showed an alteration in EAT gene expression in CAD patients with significant upregulation of MCP-1. Further studies with a large sample need to be done to confirm these findings.
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