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Related Experiment Videos

Increased cardiac fatty acid uptake with dobutamine infusion in swine is accompanied by a decrease in malonyl CoA

J L Hall1, G D Lopaschuk, A Barr

  • 1Section of Cardiovascular Pharmacology, Syntex Discovery Research, PaloAlto, CA 94304, USA.

Cardiovascular Research
|November 1, 1996
PubMed
Summary

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Increased cardiac work lowers malonyl CoA levels, boosting fatty acid uptake in the heart. This metabolic shift enhances energy transduction but isn't driven by reduced acetyl CoA carboxylase activity.

Area of Science:

  • Cardiovascular Physiology
  • Metabolic Regulation
  • Cardiac Energy Metabolism

Background:

  • Malonyl CoA regulates cardiac fatty acid oxidation by inhibiting carnitine palmitoyltransferase 1 (CPT 1).
  • Acetyl CoA carboxylase (ACC) produces malonyl CoA from acetyl CoA.
  • Understanding malonyl CoA's role is crucial for addressing altered cardiac energy transduction.

Purpose of the Study:

  • To investigate if changes in malonyl CoA regulation contribute to increased cardiac energy transduction during elevated cardiac work.
  • To determine the impact of dobutamine-induced cardiac work on malonyl CoA levels and fatty acid metabolism.

Main Methods:

  • Anesthetized swine underwent a control period followed by dobutamine or saline infusion.
  • Cardiac function, myocardial oxygen consumption (MVO2), and substrate uptake were measured.

Related Experiment Videos

  • Malonyl CoA content, ACC activity, and AMP-dependent protein kinase (AMPK) activity were assessed.

    • Main Results:

    • Dobutamine significantly increased heart rate, cardiac contractility, and MVO2.
    • Free fatty acid and glucose uptake increased by 210% and 248%, respectively, with dobutamine.
    • Malonyl CoA content decreased by 55% with dobutamine, while ACC and AMPK activities remained unchanged.

    Conclusions:

    • Increased cardiac work, induced by dobutamine, is associated with reduced malonyl CoA levels and enhanced fatty acid uptake.
    • The observed decrease in malonyl CoA is not mediated by reduced ACC activity.
    • These findings suggest a complex regulatory mechanism for cardiac energy metabolism during increased workload.