Incomplete Palmitate Oxidation: Possible Source of Human Myopathy

Jack B. Shumate, Michael H. Brooke, James Edwin Carroll, Rati M. Choksi

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

A study of palmitate oxidation in 200 consecutive human muscle biopsy specimens showed 14 patients in whom there was abnormal, incomplete palmitate oxidation when the rate of oxidation of palmitate14C (ul) was compared with that of palmitate14C (at carbon 1). Five patients had denervation as a primary diagnosis, and the remaining nine had a primary muscle disease. Of this latter group, six had clinical similarities, including proximal weakness, necrotic fibers on muscle biopsy, and extreme elevations of serum creatine kinase. With one exception, lipid storage was not part of the syndrome. The possibility of incomplete palmitate oxidation due to a defect in β-oxidation producing a human myopathy is discussed.

Original languageEnglish (US)
Pages (from-to)561-564
Number of pages4
JournalArchives of Neurology
Volume39
Issue number9
DOIs
StatePublished - Jan 1 1982
Externally publishedYes

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Palmitates
Muscular Diseases
Muscles
Biopsy
Denervation
Creatine Kinase
Carbon
Lipids
Serum
Oxidation
Incomplete

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

Cite this

Incomplete Palmitate Oxidation : Possible Source of Human Myopathy. / Shumate, Jack B.; Brooke, Michael H.; Carroll, James Edwin; Choksi, Rati M.

In: Archives of Neurology, Vol. 39, No. 9, 01.01.1982, p. 561-564.

Research output: Contribution to journalArticle

Shumate, Jack B. ; Brooke, Michael H. ; Carroll, James Edwin ; Choksi, Rati M. / Incomplete Palmitate Oxidation : Possible Source of Human Myopathy. In: Archives of Neurology. 1982 ; Vol. 39, No. 9. pp. 561-564.
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