title: Myocardial dysfunction in an animal model of cancer cachexia.
abstract: OBJECTIVE
  Fatigue is a common occurrence in cancer patients regardless of tumor type or anti-tumor therapies and is an especially problematic symptom in persons with incurable tumor disease. In rodents, tumor-induced fatigue is associated with a progressive loss of skeletal muscle mass and increased expression of biomarkers of muscle protein degradation. The purpose of the present study was to determine if muscle wasting and expression of biomarkers of muscle protein degradation occur in the hearts of tumor-bearing mice, and if these effects of tumor growth are associated with changes in cardiac function.
  
  
  METHODS
  The colon26 adenocarcinoma cell line was implanted into female CD2F1 mice and skeletal muscle wasting, in vivo heart function, in vitro cardiomyocyte function, and biomarkers of muscle protein degradation were determined.
  
  
  RESULTS
  Expression of biomarkers of protein degradation were increased in both the gastrocnemius and heart muscle of tumor-bearing mice and caused systolic dysfunction in vivo. Cardiomyocyte function was significantly depressed during both cellular contraction and relaxation.
  
  
  CONCLUSIONS
  These results suggest that heart muscle is directly affected by tumor growth, with myocardial function more severely compromised at the cellular level than what is observed using echocardiography.
authors.affiliation: College of Nursing, The Ohio State University, United States.
authors.forename: Hui
authors.initials: H
authors.lastname: Xu
authors.forename: Danielle
authors.initials: D
authors.lastname: Crawford
authors.forename: Kirk R
authors.initials: KR
authors.lastname: Hutchinson
authors.forename: Dane J
authors.initials: DJ
authors.lastname: Youtz
authors.forename: Pamela A
authors.initials: PA
authors.lastname: Lucchesi
authors.forename: Markus
authors.initials: M
authors.lastname: Velten
authors.forename: Donna O
authors.initials: DO
authors.lastname: McCarthy
authors.forename: Loren E
authors.initials: LE
authors.lastname: Wold
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002100:Cachexia / Q000209:etiology / Q000378:metabolism*; D009202:Cardiomyopathies / Q000378:metabolism*; D003110:Colonic Neoplasms / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000737:chemistry / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism; D009368:Neoplasm Transplantation; D012333:RNA, Messenger / Q000378:metabolism; D044843:SKP Cullin F-Box Protein Ligases / Q000235:genetics / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms
chemical_list: C508686:BNip3 protein, mouse; D015415:Biomarkers; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D009124:Muscle Proteins; D012333:RNA, Messenger; C486692:Fbxo32 protein, rat; D044843:SKP Cullin F-Box Protein Ligases