Increased long chain acyl CoA in duchenne muscular dystrophy

James E. Carroll, Aida Villadiego, Michael H. Brooke

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)1507-1510
Number of pages4
JournalNeurology
Volume33
Issue number11
StatePublished - Nov 1983
Externally publishedYes

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ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Carroll, J. E., Villadiego, A., & Brooke, M. H. (1983). Increased long chain acyl CoA in duchenne muscular dystrophy. Neurology, 33(11), 1507-1510.