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Kinetics of carnitine-dependent fatty acid oxidation

Implications for human carnitine deficiency

Departments of Internal Medicine (Drs. Long, Foster, and McGarry), Biochemistry (Dr. McGarry), and Neurology (Dr. Haller), the University of Texas Health Science Center at Dallas, Dallas. TX.

The relationship between the concentration of carnitine and the oxidation of oleate was examined in homogenates prepared from skeletal muscle, liver, kidney, and heart of the rat, and from canine and human skeletal muscle. The carnitine content of these tissues in situ spanned a wide range, from about 0.1 µmol per gram in rat liver to about 3.0 µmol per gram in human muscle. The concentration of carnitine required for half-maximal rates of fatty acid oxidation in vitro also varied greatly (10 to 15 µM for rat liver to 200 to 400 µM for human muscle), and in rough proportion to the normal carnitine content of the tissues. For any given tissue, the carnitine content seems to be set at a level necessary for optimal rates of fatty acid oxidation. The data provide a plausible explanation for the fact that muscle fatty acid metabolism is severely impaired in the syndrome of human carnitine deficiency, since measured carnitine levels are in the range expected to limit substantially the capacity for fatty acid oxidation.

Address correspondence and reprint requests to Dr. McGarry, Department of Internal Medicine, the University of Texas Health Science Center at Dallas, Dallas, TX 75235.

This work was supported by grants from the US Public Health Service (AM 18573) and the Morgan Good Foundation.

Presented in part at the thirty-third annual meeting of the American Academy of Neurology, Toronto, Canada, May 1981.

Accepted for publication November 10, 1981

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