Anagha Vinay Sahasrabuddhe

Background & objectives: Coronary 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. Methods: Twenty 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. Results: Leptin levels were significantly higher in CABG group as compared to controls (PMCP-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 (PMCP-1. Further studies with a large sample need to be done to confirm these findings.

The burden of obesity and associated disorders is ever-increasing in modern lifestyle. Obesity is strongly associated with increase in all-cause mortality. Obesity results from chronic positive energy balance. Excess fat is stored in two compartments: subcutaneous andvisceral. Of these, major chunk of fat 80% is deposited subcutaneously while a smaller percentage as visceral fat depot. Continued accumulation of adipose tissue leads to initially hypertrophy and later visceral accumulation. In the initial stages of development ofobesity, subcutaneous adipose tissue acts like a sink, protecting the organs from excess of FFAs and triglycerides but when the stress of excess caloric intake overrides the capacity of subcutaneous fat, visceral fat depot starts expanding.