Effects of carnitine supplementation on myocardial function and energy provision in experimental uraemia
| Autor: | Anne-Marie, Seymour, Veena, Reddy, Sunil, Bhandari |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Male
Cardiac function curve medicine.medical_specialty Magnetic Resonance Spectroscopy Left ventricular hypertrophy General Biochemistry Genetics and Molecular Biology Phosphocreatine Rats Sprague-Dawley chemistry.chemical_compound Carnitine Internal medicine medicine Animals Uremia Cause of death General Immunology and Microbiology business.industry Heart Metabolism medicine.disease Rats Endocrinology Biochemistry chemistry Dietary Supplements business Perfusion medicine.drug Kidney disease |
| Zdroj: | Frontiers in Bioscience. :834-844 |
| ISSN: | 1945-0508 1945-0494 |
| DOI: | 10.2741/e664 |
| Popis: | Cardiovascular complications are the leading cause of death in patients with chronic kidney disease. The uraemic heart undergoes remodelling and changes in metabolic function. Experimental uraemia produces a reduction in the myocardial energy reserve phosphocreatine in parallel with left ventricular hypertrophy and depletion of serum carnitine. This study investigated the effects of chronic L-carnitine supplementation on myocardial substrate metabolism and function in the experimental uraemia. Experimental uraemia was induced surgically in male Sprague-Dawley rats via a subtotal nephrectomy. Carnitine was administered continuously via subcutaneous mini-osmotic pumps. Cardiac function and substrate oxidation were assessed in vitro by means of isovolumic perfusion using 13C NMR, at 3 and 6 weeks. Uraemic animals exhibited anaemia, kidney dysfunction and systemic carnitine deficiency but no myocardial tissue carnitine deficiency. Myocardial hypertrophy was abolished following carnitine supplementation. This was associated with a reduction in glucose utilisation. In summary carnitine supplementation prevents cardiac hypertrophy, and this effect is amplified with the duration of treatment. This is associated with a reduction in myocardial glucose utilisation but no significant modulation of myocardial function. |
| Databáze: | OpenAIRE |
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