Abstract
Carnitine concentration in tissue is generally related to mitochondrial volume-density and ability to oxidize fatty acids. The highest tissue carnitine has been detected in ventricular myocardium which, compared to other tissues, presents elevated rates of oxidative phosphorylation [1]. The ability of cardiac mitochondria to oxidize long chain fatty acids is also much higher when compared to skeletal muscle or liver sarcosomes (Table 1). Paradoxically enough, it has been known for many years [3–5] that the heart is missing γ-butyrobetaine hydroxylase [6, 7], the last enzyme of carnitine synthesizing pathway, and that in the myocardium of different species including man, the carnitine synthesis stops at the level of deoxycarnitine (γ-butyrobetaine). The tissue presenting the highest carnitine concentrations must therefore take up this essential co-factor of lipid metabolism from the blood where it is supplied by liver and, in some species, by kidney [6, 8].
“An alteration of active carnitine transport did occur during the development of cardiac hypertrophy: both total and carrier-mediated carnitine transport were significantly depressed. The alterations of carrier-mediated transport might be related to a decreased affinity of membrane carrier for L-carnitine (higher apparent KM for carnitine) rather than to a decreased number of carriers (Vmax unchanged).”
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© 1995 Springer Science+Business Media Dordrecht
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Moravec, J., El Alaoui-Tablibi, Z., Brunold, C. (1995). Carnitine transport in volume-overloaded rat hearts. In: De Jong, J.W., Ferrari, R. (eds) The Carnitine System. Developments in Cardiovascular Medicine, vol 162. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-0275-9_10
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DOI: https://doi.org/10.1007/978-94-011-0275-9_10
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