Li, Sin-JinSin-JinLiWu, Twin-WayTwin-WayWuChien, Miao-JuMiao-JuChienMersmann, Harry JHarry JMersmannCHING-YI CHEN2019-06-182019-06-182019-071388-1981https://api.elsevier.com/content/abstract/scopus_id/85063090719https://scholars.lib.ntu.edu.tw/handle/123456789/411182Heart is a high energy demand organ and cardiac fat is the main local energy source for heart. Alteration in cardiac fat may affect cardiac energy and contribute to heart dysfunction. We previously observed a link between alteration in pericardial fat (PAT) and local adverse effects on myocardial fibrosis in obese minipigs. This study investigated the role of PAT on cardiac energy and mitochondrial function, and elucidated a potential mechanism for PAT in cardiac fibrosis.enAutophagy; High-fat diet; Minipigs; Mitochondrial dynamics; Mitochondrial respiration; Pericardial adipose tissue[SDGs]SDG3[SDGs]SDG7adenosine triphosphate; malonaldehyde; saturated fatty acid; adult; animal experiment; animal model; apoptosis; Article; cell function; controlled study; diet induced obesity; disease course; disorders of mitochondrial functions; energy metabolism; female; H9c2(2-1) cell line; heart left ventricle; heart muscle fibrosis; lipid diet; male; mitochondrial respiration; mitochondrion; mitophagy; nonhuman; pericardial fat; priority journal; protein expression; adipose tissue; adverse event; animal; cardiac muscle cell; cell line; complication; conditioned medium; cytology; fibrosis; metabolism; minipig; mitochondrion; obesity; paracrine signaling; pericardium; pharmacology; physiology; pig; Adipose Tissue; Animals; Apoptosis; Cell Line; Culture Media, Conditioned; Diet, High-Fat; Fibrosis; Mitochondria; Myocytes, Cardiac; Obesity; Paracrine Communication; Pericardium; Swine; Swine, Miniaturejournal article10.1016/j.bbalip.2019.03.004308721202-s2.0-85063090719WOS:000467664400001https://api.elsevier.com/content/abstract/scopus_id/85063090719