Abstract 17549: Human Epicardial Fat Shares Molecular and Morphologic Features of Omental Fat
Introduction: Epicardial adipose tissue (EAT) has been postulated to play a direct role in obesity associated cardiovascular disease. However, the majority of observational studies have shown that when controlling for visceral adipose tissue (VAT), there is no independent CV risk imparted by EAT.
Hypothesis: We tested the hypothesis that the set of differentially expressed genes between subcutaneous adipose tissue (SAT) and EAT would be similar to that found when comparing SAT and VAT.
Methods: RNA was prepared from paired fat samples taken from patients having valve surgery (n=9) or gastric bypass (n=8). Diabetic patients were excluded and patients were matched for insulin sensitivity using HOMA-IR2. Gene expression in paired SAT/EAT or SAT/VAT was compared using Affymetrix Human Gene 1.0 chips. Adipocyte size was measured using automated tracing of adipocyte area.
Results: Cardiac surgery patients were more frequently male, had a lower BMI, and were older (p<0.05); there was no difference in HOMA-IR2 between groups. Expression of 189 genes was significantly different (FC>2.0, p<0.05) between SAT and EAT whereas expression of 1334 genes was different between SAT and VAT (Fig 1, Top). Of the 189 genes differentially expressed in EAT vs. SAT, 46% were commonly differentially expressed in VAT vs. SAT. These included the canonical VAT specific genes TCF21, ITLN1, SRFP2, and TBX15. Similar to VAT, adipocyte size in EAT was significantly smaller than SAT in both patients with and without coronary disease (Fig 1, Bottom).
Conclusions: EAT exhibits a transcriptional profile similar to VAT, including increased expression of canonical VAT specific genes. Adipocytes from EAT are also smaller than those from SAT. This is the first molecular study to confirm clinical studies which suggest that EAT is similar to VAT. However, 54% of the differentially expressed genes in EAT vs. SAT are unique to this depot, and these may confer an independent influence of EAT to CV risk.
- © 2013 by American Heart Association, Inc.