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Increased long chain acyl CoA in Duchenne muscular dystrophy

Departments of Pediatrics and Neurology, and Neurosurgery (Neurology), Washington University School of Medicine, Saint Louis, MO.

Compared with normal or denervated human muscle, long chain acyl CoA was increased in muscle from patients with Duchenne dystrophy. Free and short chain acylcarnitine were reduced in Duchenne muscle, whereas long chain acylcarnitine was preserved. The accumulation of long chain fatty acid derivatives may imply disruption of fatty acid oxidation.

Address correspondence and reprint requests to Dr. Carroll, Department of Neurology, Box 8111, 660 South Euclid, Washington University School of Medicine, Saint Louis, MO 63110.

Supported by a Center Grant from the Muscular Dystrophy Association. Dr. Carroll is the recipient of NIH Teacher-Investigator Award 5-K07-NS00386.

Presented in part at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, April 1982.

Accepted for publication March 22, 1983

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