Bénédicte Gaborit1, Nicolas Venteclef2, Patricia Ancel1, Véronique Pelloux3, Vlad Gariboldi4, Pascal Leprince5, Julien Amour5, Stéphane N Hatem6, Elisabeth Jouve7, Anne Dutour8, Karine Clément9. 1. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France INSERM, Nutriomics (team6 and Team3), UMR_S U1166, Paris F-75013, France Aix-Marseille Université, Faculté de Médecine, Department 'Nutrition, Obésité et Risque Thrombotique', INSERM, UMR 1062, INRA 1260, 13385 Marseille, France. 2. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France INSERM, UMRS_S1138, Paris F-75006, France. 3. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France INSERM, Nutriomics (team6 and Team3), UMR_S U1166, Paris F-75013, France. 4. Assistance-Publique Hôpitaux de Marseille, Cardiac Surgery, La Timone Hospital,13005 Marseille, France. 5. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Heart Department, 73013 Paris, France. 6. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France INSERM, Nutriomics (team6 and Team3), UMR_S U1166, Paris F-75013, France Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Heart Department, 73013 Paris, France. 7. Assistance-Publique Hôpitaux de Marseille, Medical Evaluation Department, CIC-CPCET, 13005 Marseille, France. 8. Aix-Marseille Université, Faculté de Médecine, Department 'Nutrition, Obésité et Risque Thrombotique', INSERM, UMR 1062, INRA 1260, 13385 Marseille, France anne.dutour@ap-hm.fr karine.clement@psl.aphp.fr. 9. Institute of Cardiometabolism and Nutrition, ICAN, Heart and Nutrition Department, Assistance-Publique Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris F-75013, France Sorbonne Universities, University Pierre et Marie Curie-Paris 6, UMRS 1166, Paris F-75006, France INSERM, Nutriomics (team6 and Team3), UMR_S U1166, Paris F-75013, France anne.dutour@ap-hm.fr karine.clement@psl.aphp.fr.
Abstract
AIMS: Human epicardial adipose tissue (EAT) is a visceral and perivascular fat that has been shown to act locally on myocardium, atria, and coronary arteries. Its abundance has been linked to coronary artery disease (CAD) and atrial fibrillation. However, its physiological function remains highly debated. The aim of this study was to determine a specific EAT transcriptomic signature, depending on its anatomical peri-atrial (PA), peri-ventricular (PV), or peri-coronary location. METHODS AND RESULTS: Samples of EAT and thoracic subcutaneous fat, obtained from 41 patients paired for cardiovascular risk factors, CAD, and atrial fibrillation were analysed using a pangenomic approach. We found 2728 significantly up-regulated genes in the EAT vs. subcutaneous fat with 400 genes being common between PA, PV, and peri-coronary EAT. These common genes were related to extracellular matrix remodelling, inflammation, infection, and thrombosis pathways. Omentin (ITLN1) was the most up-regulated gene and secreted adipokine in EAT (fold-change >12, P < 0.0001). Among EAT-enriched genes, we observed different patterns depending on adipose tissue location. A beige expression phenotype was found in EAT but PV EAT highly expressed uncoupled protein 1 (P = 0.01). Genes overexpressed in peri-coronary EAT were implicated in proliferation, O-N glycan biosynthesis, and sphingolipid metabolism. PA EAT displayed an atypical pattern with genes implicated in cardiac muscle contraction and intracellular calcium signalling pathway. CONCLUSION: This study opens new perspectives in understanding the physiology of human EAT and its local interaction with neighbouring structures. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Human epicardial adipose tissue (EAT) is a visceral and perivascular fat that has been shown to act locally on myocardium, atria, and coronary arteries. Its abundance has been linked to coronary artery disease (CAD) and atrial fibrillation. However, its physiological function remains highly debated. The aim of this study was to determine a specific EAT transcriptomic signature, depending on its anatomical peri-atrial (PA), peri-ventricular (PV), or peri-coronary location. METHODS AND RESULTS: Samples of EAT and thoracic subcutaneous fat, obtained from 41 patients paired for cardiovascular risk factors, CAD, and atrial fibrillation were analysed using a pangenomic approach. We found 2728 significantly up-regulated genes in the EAT vs. subcutaneous fat with 400 genes being common between PA, PV, and peri-coronary EAT. These common genes were related to extracellular matrix remodelling, inflammation, infection, and thrombosis pathways. Omentin (ITLN1) was the most up-regulated gene and secreted adipokine in EAT (fold-change >12, P < 0.0001). Among EAT-enriched genes, we observed different patterns depending on adipose tissue location. A beige expression phenotype was found in EAT but PV EAT highly expressed uncoupled protein 1 (P = 0.01). Genes overexpressed in peri-coronary EAT were implicated in proliferation, O-N glycan biosynthesis, and sphingolipid metabolism. PA EAT displayed an atypical pattern with genes implicated in cardiac muscle contraction and intracellular calcium signalling pathway. CONCLUSION: This study opens new perspectives in understanding the physiology of human EAT and its local interaction with neighbouring structures. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Luisa Ciuffo; Hieu Nguyen; Mateus Diniz Marques; Konstantinos N Aronis; Bhradeev Sivasambu; Henrique D de Vasconcelos; Susumu Tao; David D Spragg; Joseph E Marine; Ronald D Berger; Joao A C Lima; Hugh Calkins; Hiroshi Ashikaga Journal: Circ Cardiovasc Imaging Date: 2019-06-10 Impact factor: 7.792
Authors: Chris T Longenecker; Seunghee Margevicius; Yiying Liu; Mark D Schluchter; Chun-Ho Yun; Hiram G Bezerra; Grace A McComsey Journal: Am J Cardiol Date: 2017-07-24 Impact factor: 2.778
Authors: Kanta Chechi; Jinchu Vijay; Pierre Voisine; Patrick Mathieu; Yohan Bossé; Andre Tchernof; Elin Grundberg; Denis Richard Journal: JCI Insight Date: 2019-04-18