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Myocardial dysfunction in an animal model of cancer cachexia
Author(s) -
Youtz Dane J,
Hutchinson Kirk R,
Velten Markus,
Xu Hui,
Gorr Matthew,
Lucchesi Pamela A,
McCarthy Donna O,
Wold Loren E
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1112.12
Subject(s) - cachexia , wasting , medicine , skeletal muscle , heart failure , in vivo , cancer , protein degradation , myocyte , endocrinology , pathology , cardiology , oncology , biology , microbiology and biotechnology
Aims Fatigue is a common syndrome in cancer patients independent of anti‐tumor therapies or tumor type and is a 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 the 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 cardiac dysfunction. Main Methods The colon 26 adenocarcinoma cell line was implanted into female CD2F1 mice and the amount of skeletal muscle wasting, in vivo heart function, in vitro cardiomyocyte function, and biomarkers of muscle protein degradation were determined. Key Findings The expression of biomarkers of protein degradation were increased in both the gastrocnemius and heart muscle of tumor‐bearing mice and associated with systolic dysfunction in vivo. Cardiomyocyte function was significantly depressed during both cellular contraction and relaxation. Significance 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 clinical methods.