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Before fatty acids can be metabolized for energy they must be transported into the mitochondria, and before the end products of fatty acid decomposition (acetyl groups) can be used in the body for energy or to make carbohydrates they must be transported out of the mitochondria. Carnitine promotes the movement of those important molecules. Without carnitine, the metabolism of fatty acids would slow as would the utilization of the acetyl groups, which are the end products of fatty acid metabolism. This would limit the amount of energy that can be obtained from fats. Carnitine has become the centre of attention in recent years because of the its potential to improve performance and, perhaps, assist in the management of myocardial pathology.

Dogs and cats both make carnitine from the amino acid lysine and, therefore, it is unlikely that simple dietary deficiencies exist in the normal animal. There does, however, appear to be a connection between diet and plasma levels of carnitine. Dogs given a plant protein-based diet had plasma carnitine levels that are 50% of those measured in dogs fed animal-protein based diets. This suggests that plasma levels of carnitine are susceptible to dietary intake. However, there is little evidence that tissue concentrations can be influenced by diet in normal animals.

While a direct connection between carnitine intake and a deficiency syndrome is difficult to establish in normal animals, there are reports of carnitine deficiency being linked to myocardial disorders in dogs(1) such as dilated cardiomyopathy (DCM) in Boxers, Doberman Pinchers and American Cocker Spaniels (2), (3). In these studies, 80% of the dogs with DCM had elevated plasma carnitine levels, yet had depressed myocardial concentrations. This suggests that there may be a problem in these animals with the mechanism that transfers carnitine into the heart. There was no difference in clinical outcome between DCM dogs supplemented with carnitine and DCM dogs receiving no supplementation in studies by Costa and Labuc(4). Those dogs receiving carnitine supplementation had significantly higher myocardial carnitine levels than the non-supplemented group, but this had no correlation with the clinical outcome of the disease. The fact that supplementation increases myocardial carnitine levels without reversal of DCM would make carnitine deficiency as a causal factor in DCM unlikely.

Rodriques et al.(5) noted that fasting in dogs changed the pattern of utilization of carnitine. Fasting increased plasma carnitine concentrations without corresponding changes in the levels of carnitine found in muscle tissue. In the fasting animal, long chain fatty acids are an important energy source and must be coupled with carnitine for transport into the mitochondria for oxidation. Prolonged fasting resulted in rising levels of carnitine in muscle tissue due to disruption in normal enzymatic metabolic pathways. One of the effects of DCM is a loss of appetite and decreased food intake, implying one possible explanation for the apparent changes in tissue carnitine concentrations in DCM as a result of fasting.

Pet food makers are adding supplementary carnitine to weight management and performance diets. Carnitine is added to weight management diets to support the increased amount of fat metabolism associated with loss of adipose tissue. In the case of performance diets, carnitine is added to the diet to support the 500% increase in muscle carnitine which occurs under heavy work (6), (7). The practical effects of adding supplementary carnitine in both weight management and performance diets have not been well demonstrated.

Normal canines appear to make enough carnitine to meet their usual requirements. Carnitine has been implicated in DCM but supplementary carnitine does not affect the clinical outcome of DCM. Supplementary carnitine may be added to weight management and performance diets to facilitate the metabolism of fats and release of energy. The efficacy of these treatments remains to be definitively established.

1. Stepian RL, Miller MW. Cardiovascular disease. In: Wills JM, Simpson KW eds. The Waltham Book of Clinical Nutrition of Dog, Oxford, Pergamon Press, 1994: 353-371.

2. Keene BW, Panciera DP, Atkins CE, Regitz V, Schmidt MJ, Shug AL. Myocardial L-carnitine in a family of dogs with dilated cardiomyopathy. JAVMA 1991; 198: 647-650.

3. Keene BW, Mier HC, Meura KM, Schmidt MJ, Shug AL. Dietary L-carnitine concentration in dogs. Proc. Ninth Annual ACVIM Forum p. 890 (abstr).

4. Costa ND, Labuc RH. Case report: efficacy of oral carnitine therapy for dilated cardiomyopathy in boxer dogs. J. Nutr 1994; 124:2687s-2692s.

5. Rodriques J, Bruyns J, Askanazi J, DiMaugo W, Bordley JIV, Edwin DH, Kinney JW. Carnitine metabolism during fasting in dogs. Surgery 1986; 99:684-687.

6. Hiatt WR, Regensteiner JG, Wolfel EE, Ruff L, Brass EP. Carnitine and acylcarnitine metabolism during exercise in humans. Dependence on skeletal muscle metabolic state. J. Clin Invest 1989; 84: 1167-1173.

7. Friolet R, Hoeppler H, Krähenbühl S, Relationship between coenzyme A and carnitine pools in human skeletal muscle at rest and after exhaustive exercise under normoxic and acutely hypoxic conditions. J Clin Invest 1994; 94:1490-1495.

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