Adipose tissue present between the heart and visceral layer of the pericardium, i.e. in direct contact with the heart, is known as epicardial adipose tissue (EAT) and is located primarily near the coronary vessels. It has been proposed that it has a role in lipid storage as well as limiting the impact of torsion forces through the cardiac cycle (Keegan et al 2004). The brown adipose tissue (BAT) specific gene uncoupling protein (UCP)1, and other BAT related genes, are all highly expressed in EAT (Sacks et al. 2009). The aim of the present study was to quantify the amount of UCP1 within EAT and to compare this with paracardial and subcutaneous adipose tissue (SAT) depots from the same individuals. Method: Adipose tissue samples were obtained from 6 females and 2 males aged between 58-74 years and with a body mass index between 26.6-38.3 kg/m2. Mitochondria were prepared from ~200mg of adipose tissue (Symonds et al. 1992) and abundance of UCP1 was determined by immunoblotting using a rabbit polyclonal antibody to human UCP1 (Abcam, Cambridge, U.K.). Specificity of the detection was confirmed using non-immune rabbit serum and a range of molecular-weight markers was included on all gels. All gels were run in duplicate and reference samples (i.e. from either BAT or the liver (negative control) of a 6 hour old sheep) were included on each gel to allow comparison between each group. Results: UCP1 was highly abundant in all EAT samples but was absent from paracardial fat and was only found in the sternal depot of subcutaneous fat. The mean ± SEM optical density of from all EAT samples was 0.77 ± 0.0.28 compared with 0.23 ± 0.11 arbitrary units for sternal SAT (p<0.05). UCP1 protein was undetectable in paracardial fat as well as upper abdominal and lower extremity SAT. Discussion: UCP1 is present in significant amounts within human EAT, thereby confirming it is a BAT depot in adult humans. This raises the possibility that EAT can have a thermoregulatory function in the heart, possibly protecting against hypothermia. BAT also influences vascular lipoprotein homeostasis by inducing triglyceride rich lipoprotein turnover and channelling lipids (Bartlet el al. 2011) and could protect the heart against toxic levels of fatty acids in the coronary circulation.