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Abnormalities in the catabolic fate of long‐chain fatty acids and glucose in compensated murine cardiac hypertrophy
Author(s) -
Wambolt Richard B,
Parsons Hannah L,
Bohunek Lubos,
Allard Michael F
Publication year - 2008
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.22.1_supplement.751.4
Subject(s) - catabolism , medicine , endocrinology , muscle hypertrophy , fatty acid , metabolism , chemistry , in vivo , biology , islet , beta oxidation , insulin , biochemistry , microbiology and biotechnology
Reduced oxidative catabolism of fatty acids (FAO) and accelerated rates of non‐oxidative glucose catabolism (NOG) are recognized metabolic abnormalities in genetic and acquired models of cardiac hypertrophy (H) in rats, but are less well characterized in mice. We determined catabolic fates of long‐chain fatty acid (palmitate – P) and glucose (G) in compensated non‐hypertrophied (C) and hypertrophied (H) hearts from sham‐operated and abdominal aortic‐constricted CD1 mice. Hearts were perfused with either 1.2mM P, 5.5mM G, 0.5mM lactate and 20mU/L insulin (Series 1) or 0.6mM P, 5.5mM G, 1.5mM lactate, 0.5mM pyruvate and 20mU/L insulin (Series 2 ‐ reflects in vivo substrate concentrations in mice). No differences in heart function, expressed as cardiac power (ml·mmHg·min −1 ), were observed between C and H in either Series 1 (10.9 ± 0.6 vs. 10.4 ± 0.3) or Series 2 (12.8 ± 0.4 vs. 13.1 ± 0.6). Results: Substrate catabolism in a murine model of acquired compensated H resembles that in models of H in rats. Abnormalities in NOG persist in hearts exposed to a physiologically relevant substrate mixture, even though significant differences in FAO disappear, suggesting that defects in NOG are a key metabolic abnormality occurring early in the development of H.