title: Carnitine regulates myocardial metabolism by Peroxisome Proliferator-Activated Receptor-alpha (PPARalpha) in alcoholic cardiomyopathy.
abstract: BACKGROUND
  Chronic alcohol intake exerts myocardial damage en route to the development of alcoholic cardiomyopathy (ACM), although the precise pathogenesis of ACM is unknown. Carnitine is known to participate in the regulation of metabolism in a number of heart diseases. This study was designed to examine the interplay between myocardial metabolism and carnitine in the development of ACM.
  
  
  METHODS
  Experimental animals were divided into 3 groups: (i) group A: alcohol-fed. (ii) group B: alcohol/carnitine: (200mg/kg/d, p.o. by mixing carnitine in rat chow). (iii) group C: control. Blood levels of free fatty acid (FFA), total carnitine (TC) and free carnitine (FC) were monitored in rats receiving alcohol with or without carnitine. Mitochondrial adenine nucleotide translocator-1 (ANT1) activity, ATPase activity, high energy phosphate concentration, peroxisome proliferator-activated receptor-α (PPARα), carnitine-palmitoyl transferase I (CPT-I), medium-chain acyl-coenzyme A dehydrogenase (MCAD), ANT1 and ATPase mRNA and protein expression were also monitored in myocardial tissue.
  
  
  RESULTS
  Experimental animals received alcohol with or without carnitine for six 6 months. Our results indicated that FFA increased abruptly. TC and FC were significantly decreased in groups receiving alcohol at 4 months. The concentration of ATP, ADP and AMP in the myocardium decreased following 2 months of alcohol administration. mRNA and protein expression of PPARα, CPT-I, MCAD, ANT1 and ATPase expressions were gradually altered in groups following alcohol feeding.
  
  
  CONCLUSIONS
  These observations suggest that abnormal metabolism is present in the myocardium during the development of ACM. Carnitine may improve myocardial metabolism by elevating the content of PPARα, CPT-I and MCAD.
authors.affiliation: Department of Cardiology, First Clinical College of Harbin Medical University, Harbin, China. jing.ling.0451@163.com
authors.forename: Ling
authors.initials: L
authors.lastname: Jing
authors.forename: Li-jun
authors.initials: LJ
authors.lastname: Zhou
authors.forename: Wei-min
authors.initials: WM
authors.lastname: Li
authors.forename: Feng-min
authors.initials: FM
authors.lastname: Zhang
authors.forename: Lin
authors.initials: L
authors.lastname: Yuan
authors.forename: Shuang
authors.initials: S
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Song
authors.forename: Ying
authors.initials: Y
authors.lastname: Sang
mesh_terms: D042964:Acyl-CoA Dehydrogenase / Q000378:metabolism; D033741:Adenine Nucleotide Translocator 1 / Q000378:metabolism; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002310:Cardiomyopathy, Alcoholic / Q000378:metabolism*; D002331:Carnitine / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D000431:Ethanol; D005230:Fatty Acids, Nonesterified / Q000097:blood; D008854:Microscopy, Electron; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D047493:PPAR alpha / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D051381:Rats
chemical_list: D033741:Adenine Nucleotide Translocator 1; D005230:Fatty Acids, Nonesterified; D047493:PPAR alpha; D010710:Phosphates; D000431:Ethanol; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D042964:Acyl-CoA Dehydrogenase; D002334:Carnitine O-Palmitoyltransferase; D000251:Adenosine Triphosphatases; D002331:Carnitine