title: Regional evidence of modulation of cardiac adiponectin level in dilated cardiomyopathy: pilot study in a porcine animal model.
abstract: BACKGROUND
  The role of systemic and myocardial adiponectin (ADN) in dilated cardiomyopathy is still debated. We tested the regulation of both systemic and myocardial ADN and the relationship with AMP-activated protein kinase (AMPK) activity in a swine model of non-ischemic dilated cardiomyopathy.
  
  
  RESULTS
  Cardiac tissue was collected from seven instrumented adult male minipigs by pacing the left ventricular (LV) free wall (180 beats/min, 3 weeks), both from pacing (PS) and opposite sites (OS), and from five controls. Circulating ADN levels were inversely related to global and regional cardiac function. Myocardial ADN in PS was down-regulated compared to control (p < 0.05), yet ADN receptor 1 was significantly up-regulated (p < 0.05). No modifications of AMPK were observed in either region of the failing heart. Similarly, myocardial mRNA levels of PPARγ, PPARα, TNFα, iNOS were unchanged compared to controls.
  
  
  CONCLUSIONS
  Paradoxically, circulating ADN did not show any cardioprotective effect, confirming its role as negative prognostic biomarker of heart failure. Myocardial ADN was reduced in PS compared to control in an AMPK-independent fashion, suggesting the occurrence of novel mechanisms by which reduced cardiac ADN levels may regionally mediate the decline of cardiac function.
authors.affiliation: Consiglio Nazionale delle Ricerche (CNR), Institute of Clinical Physiology, Laboratory of Cardiovascular Biochemistry, Pisa, Italy.
authors.forename: Chiara
authors.initials: C
authors.lastname: Caselli
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Lionetti
authors.forename: Manuela
authors.initials: M
authors.lastname: Cabiati
authors.forename: Tommaso
authors.initials: T
authors.lastname: Prescimone
authors.forename: Giovanni D
authors.initials: GD
authors.lastname: Aquaro
authors.forename: Virginia
authors.initials: V
authors.lastname: Ottaviano
authors.forename: Fabio
authors.initials: F
authors.lastname: Bernini
authors.forename: Letizia
authors.initials: L
authors.lastname: Mattii
authors.forename: Silvia
authors.initials: S
authors.lastname: Del Ry
authors.forename: Daniela
authors.initials: D
authors.lastname: Giannessi
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D052242:Adiponectin / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D015536:Down-Regulation; D006333:Heart Failure / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000473:pathology*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010865:Pilot Projects; D012333:RNA, Messenger / Q000378:metabolism; D054419:Receptors, Adiponectin / Q000378:metabolism; D013318:Stroke Volume; D013552:Swine; D013556:Swine, Miniature; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D052242:Adiponectin; D047493:PPAR alpha; D047495:PPAR gamma; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; D055372:AMP-Activated Protein Kinases