IMR Press / FBE / Volume 5 / Issue 3 / DOI: 10.2741/E664

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Cardiac effects of carnitine supplementation in experimental uraemia

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1 Department of Biological Sciences and Hull York Medical School, University of Hull, Kingston-upon-Hull, United Kingdom
2 Department of Renal Medicine, Hull and East Yorkshire Hospital NHS Trust, and Hull York Medical School Kingston-uponHull, United Kingdom

*Author to whom correspondence should be addressed.

Academic Editor: Sunil Bhandari

Front. Biosci. (Elite Ed) 2013, 5(3), 834–844;
Published: 1 June 2013
(This article belongs to the Special Issue Cardiac remodelling in uraemic heart disease)

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.

Chronic Kidney Disease
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