Compensated cardiac hypertrophy is characterised by a decline in palmitate oxidation
Akki, Ashwin; Smith, Katie; Seymour, Anne Marie L.
Anne Marie L. Seymour A.M.Seymour@hull.ac.uk
Cardiac hypertrophy is an independent risk factor in the development of heart failure. However, the cellular mechanisms underlying the transition from compensated hypertrophy to heart failure are incompletely understood. The aim of this study was to investigate changes in myocardial substrate utilisation and function in pressure-overload hypertrophy (using C-13 NMR spectroscopy) in parallel with alterations in the expression pattern of genes involved in cardiac fatty acid and glucose uptake and oxidation. Left ventricular hypertrophy was induced surgically in Sprague-Dawley rats by inter-renal aortic constriction. Nine weeks later, hearts were perfused in the isovolumic mode with a physiological mixture of substrates including 5 mM 1-C-13 glucose, 1 mM 3-C-13 lactate, 0.1 mM U-C-13 pyruvate and 0.3 mM U-C-13 palmitate and cardiac function monitored simultaneously. Real-time PCR was used to determine mRNA levels of PPAR alpha and PPAR alpha-regulated metabolic enzymes. Results showed that at the stage of compensated hypertrophy, fatty acid oxidation (FAO) and expression of genes involved in FAO were markedly reduced, whilst pyruvate oxidation was enhanced, highlighting the fact that metabolic remodelling is an early event in the development of cardiac hypertrophy.
Akki, A., Smith, K., & Seymour, A. M. L. (2008). Compensated cardiac hypertrophy is characterised by a decline in palmitate oxidation. Molecular and Cellular Biochemistry, 311(1-2), 215-224. doi:10.1007/s11010-008-9711-y
|Journal Article Type||Article|
|Acceptance Date||Apr 30, 2008|
|Online Publication Date||Feb 16, 2008|
|Publication Date||Apr 1, 2008|
|Journal||MOLECULAR AND CELLULAR BIOCHEMISTRY|
|Peer Reviewed||Peer Reviewed|
|Keywords||Clinical Biochemistry; Cell Biology; Molecular Biology; General Medicine|
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