Chronic inhibition of fatty acid oxidation: New model of diastolic dysfunction

Rubin Bressler, Richard Gay, Jack G. Copeland, Joseph J. Bahl, John Bedotto, Steven Goldman

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

The proportion of cardiac energy derived from fatty acid oxidation decreases and that derived from glucose increases during ischemia. This biochemical profile of cardiac energy production is achieved in rats and mice without ischemia by pharmacological agents such as tetradecylglycidic acid. Chronically this leads to increased cardiac stiffness, and hypertrophy in the rodent models. Elements of human cardiac dysfunction are hypothesized to develop from and/or cause similar changes in substrate utilization for energy production. For some individuals treatment that would prevent or reverse these changes may be appropriate.

Original languageEnglish (US)
Pages (from-to)1897-1906
Number of pages10
JournalLife Sciences
Volume44
Issue number25
DOIs
StatePublished - 1989

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Fatty Acids
Ischemia
Oxidation
Cardiomegaly
Rats
Rodentia
Stiffness
Pharmacology
Glucose
Acids
Substrates

ASJC Scopus subject areas

  • Pharmacology

Cite this

Chronic inhibition of fatty acid oxidation : New model of diastolic dysfunction. / Bressler, Rubin; Gay, Richard; Copeland, Jack G.; Bahl, Joseph J.; Bedotto, John; Goldman, Steven.

In: Life Sciences, Vol. 44, No. 25, 1989, p. 1897-1906.

Research output: Contribution to journalArticle

Bressler, R, Gay, R, Copeland, JG, Bahl, JJ, Bedotto, J & Goldman, S 1989, 'Chronic inhibition of fatty acid oxidation: New model of diastolic dysfunction', Life Sciences, vol. 44, no. 25, pp. 1897-1906. https://doi.org/10.1016/0024-3205(89)90401-3
Bressler, Rubin ; Gay, Richard ; Copeland, Jack G. ; Bahl, Joseph J. ; Bedotto, John ; Goldman, Steven. / Chronic inhibition of fatty acid oxidation : New model of diastolic dysfunction. In: Life Sciences. 1989 ; Vol. 44, No. 25. pp. 1897-1906.
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