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

Rubin Bressler; Richard Gay; Jack G. Copeland; Joseph J. Bahl; John Bedotto; Steve Goldman

doi:10.1016/0024-3205(89)90401-3

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

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

Medicine

Research output: Contribution to journal › Article › peer-review

41 Scopus citations

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 language	English (US)
Pages (from-to)	1897-1906
Number of pages	10
Journal	Life Sciences
Volume	44
Issue number	25
DOIs	https://doi.org/10.1016/0024-3205(89)90401-3
State	Published - 1989

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology
Pharmacology, Toxicology and Pharmaceutics(all)

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10.1016/0024-3205(89)90401-3

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title = "Chronic inhibition of fatty acid oxidation: New model of diastolic dysfunction",

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.",

author = "Rubin Bressler and Richard Gay and Copeland, {Jack G.} and Bahl, {Joseph J.} and John Bedotto and Steve Goldman",

note = "Funding Information: This research was supported by grants from NIH HL-20984-11",

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doi = "10.1016/0024-3205(89)90401-3",

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pages = "1897--1906",

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T1 - Chronic inhibition of fatty acid oxidation

T2 - New model of diastolic dysfunction

AU - Bressler, Rubin

AU - Gay, Richard

AU - Copeland, Jack G.

AU - Bahl, Joseph J.

AU - Bedotto, John

AU - Goldman, Steve

N1 - Funding Information: This research was supported by grants from NIH HL-20984-11

PY - 1989

Y1 - 1989

N2 - 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.

AB - 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.

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VL - 44

SP - 1897

EP - 1906

JO - Life Sciences

JF - Life Sciences

IS - 25

ER -

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

Abstract

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