title: Epicardial fat from guinea pig: a model to study the paracrine network of interactions between epicardial fat and myocardium?
abstract: BACKGROUND
  Epicardial adipose tissue (Epi) is a fat depot which is closely apposed on the myocardium. Several lines of evidence suggest that it is not only a lipid-storing depot, but also an active endocrine organ which secrets inflammatory cytokines and chemolines as suggested for other types of visceral fat.
  
  
  OBJECTIVE
  We selected guinea pigs which have been shown to expand Epi with age, to investigate the expansion and properties of Epi and its impact on cardiac structure and function in detail.
  
  
  RESULTS
  The amount of epicardial fat increases rapidly with age and accumulates at the aortic arch. It extends over the anterior surface of both ventricles and along the anterior and posterior branches of the coronary arteries. It also expands within the epicardium. The pattern of cytokines released by Epi is altered with age showing an up- and down-regulation of a variety of the 120 cytokines analyzed. Most prominently changed are IGFBP-4 and TIMP-2, whereas the release of adiponectin is not modified by age.
  
  
  CONCLUSIONS
  The amount of Epi is closely correlated to the amount of other types of visceral fat, to insulin resistance and other features of the metabolic syndrome, but also to cardiac hypertrophy and cardiac dysfunction. The data provide evidence that the guinea pig heart is a suitable model to analyze the interactions between Epi, heart vessels and muscle tissue. It allows identifying the influence of nutritional and metabolic alterations on the complexity of the network of locally released mediators for heart structure and function. A deeper understanding of this animal model may be helpful to analyze the interactions between Epi and the myocardium in humans-where the availability of tissue and the possibilities to modify nutritional and metabolic influences on heart are restricted-and the impact of Epi on cardiovascular risk.
authors.affiliation: Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University, Düsseldorf, Germany.
authors.forename: Janine
authors.initials: J
authors.lastname: Swifka
authors.forename: Jürgen
authors.initials: J
authors.lastname: Weiss
authors.forename: Klaus
authors.initials: K
authors.lastname: Addicks
authors.forename: Jürgen
authors.initials: J
authors.lastname: Eckel
authors.forename: Peter
authors.initials: P
authors.lastname: Rösen
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism*; D000367:Age Factors; D000818:Animals; D001092:Arachidonate 12-Lipoxygenase / Q000378:metabolism; D015153:Blotting, Western; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006168:Guinea Pigs; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000378:metabolism; D008854:Microscopy, Electron; D023421:Models, Animal; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure; D019899:Paracrine Communication / Q000502:physiology*; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism
chemical_list: D018925:Chemokines; D016207:Cytokines; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D018974:Insulin-Like Growth Factor Binding Protein 4; D019716:Tissue Inhibitor of Metalloproteinase-2; D001092:Arachidonate 12-Lipoxygenase