Abstract
BackgroundVisceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids. Cardiac visceral fat comprises mediastinal adipose tissue (MAT) and epicardial adipose tissue (EAT), and MAT is a potential biomarker of risk for obese patients.AimOur objective was to evaluate the role of EAT and MAT 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) and glucocorticoid receptor (GCR) expression in comparison with subcutaneous adipose tissue (SAT) in the development of coronary atherosclerosis in obese patients with coronary artery disease (CAD), and to assess their correlations with CD68 and fatty acids from these tissues.Methods and resultsExpression of 11β-HSD-1 and GCR was measured by qRT-PCR in EAT, MAT and SAT of thirty-one obese patients undergoing coronary artery bypass grafting due to CAD (obese CAD group) and sixteen obese patients without CAD undergoing heart valve surgery (controls). 11β-HSD-1 and GCR expression in MAT were found to be significantly increased in the obese CAD group compared with controls (p < 0.05). In the obese CAD group, 11β-HSD-1 and GCR mRNA levels were strongly correlated in MAT. Stearidonic acid was significantly increased in EAT and MAT of the obese CAD group and arachidonic acid was significantly expressed in MAT of the obese male CAD group (p < 0.05).ConclusionsWe report for the first time the increased expression of 11β-HSD-1 and GCR in MAT compared with EAT and SAT, and also describe the interrelated effects of stearidonic acid, HOMA-IR, plasma cortisol and GCR mRNA levels, explaining 40.2% of the variance in 11β-HSD-1 mRNA levels in MAT of obese CAD patients. These findings support the hypothesis that MAT contributes locally to the development of coronary atherosclerosis via glucocorticoid action.
Highlights
Visceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids
We report for the first time the increased expression of 11β-HSD-1 and glucocorticoid receptor (GCR) in mediastinal adipose tissue (MAT) compared with Epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT), and describe the interrelated effects of stearidonic acid, HOMA-IR, plasma cortisol and GCR mRNA levels, explaining 40.2% of the variance in 11β-HSD-1 mRNA levels in MAT of obese coronary artery disease (CAD) patients
We found that 11β-HSD-1 and GCR mRNA levels of obese CAD group were significantly higher in MAT compared to EAT and SAT (p < 0.05, respectively), and, 11β-HSD-1 mRNA levels in MAT and SAT were significantly different in obese CAD group compared to controls (p < 0.05 and p < 0.001, respectively)
Summary
Visceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids. Visceral fat depots are recognized as a rich source of 11beta-hydroxysteriod dehydrogenase type 1(11β-HSD-1) and adipokines such as adiponectin, resistin, inflammatory cytokines, glucocorticoids and free fatty acids (FFA) [10,11] Their important role in the pathogenesis of visceral obesity has been demonstrated by clinical and animal studies [12,13,14,15,16,17]. We aimed to compare the expression of the two major determinants of glucocorticoid action; 11β-HSD-1, known as the cortisol regenerating enzyme, and GCR in two different cardiac visceral fat depots in addition to the subcutaneous fat depots of the obese CAD group and controls This was performed in order to evaluate their contribution to the development of the coronary atherosclerosis and to study their association with metabolic and clinical parameters and fatty acid profiles from these tissues
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