Recruitment of Compensatory Pathways to Sustain Oxidative Flux With Reduced Carnitine Palmitoyltransferase I Activity Characterizes Inefficiency in Energy Metabolism in Hypertrophied Hearts
Author(s) -
Н. И. Сорокина,
J. Michael O’Donnell,
Ronald McKinney,
Kayla M. Pound,
Gebre Woldegiorgis,
Kathryn F. LaNoue,
Kalpana Ballal,
Heinrich Taegtmeyer,
Peter M. Buttrick,
E. Douglas Lewandowski
Publication year - 2007
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.106.668665
Subject(s) - medicine , carnitine , energy metabolism , oxidative metabolism , oxidative phosphorylation , endocrinology , metabolism , carnitine o palmitoyltransferase , flux (metallurgy) , oxidative stress , beta oxidation , biochemistry , biology , materials science , metallurgy
Transport rates of long-chain free fatty acids into mitochondria via carnitine palmitoyltransferase I relative to overall oxidative rates in hypertrophied hearts remain poorly understood. Furthermore, the extent of glucose oxidation, despite increased glycolysis in hypertrophy, remains controversial. The present study explores potential compensatory mechanisms to sustain tricarboxylic acid cycle flux that resolve the apparent discrepancy of reduced fatty acid oxidation without increased glucose oxidation through pyruvate dehydrogenase complex in the energy-poor, hypertrophied heart.
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