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Chronic catecholamine depletion switches myocardium from carbohydrate to lipid utilisation

A J Drake-Holland1, G J Van der Vusse, T H Roemen

  • 1Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College School of Medicine, University of London, UK. a.drake-holland@ic.ac.uk

Cardiovascular Drugs and Therapy
|October 24, 2001
PubMed

Insights

Chronic cardiac denervation increases fatty acid (FA) utilization for energy. This shift in substrate oxidation is linked to catecholamine depletion and altered pyruvate dehydrogenase activity in the heart.

Area of Science:

  • Cardiology
  • Metabolic Physiology
  • Cardiac Surgery

Background:

  • Chronic cardiac denervation, involving sympathetic and parasympathetic pathways, inhibits myocardial glucose oxidation.
  • The compensatory metabolic substrate shift in denervated hearts remains incompletely understood.

Purpose of the Study:

  • To investigate if chronic cardiac denervation leads to increased utilization of fatty acids (FA) for myocardial energy production.
  • To test the hypothesis that FA extraction and contribution to oxidative energy conversion are elevated post-denervation.

Main Methods:

  • Utilized anesthetized dogs (n=6 control, n=6 cardiac denervated) at least four weeks post-surgery.
  • Measured total fatty acid (FA) utilization and employed a radio-labeled tracer (U-14C palmitate) to quantify FA oxidation.
  • Assessed substrate oxidation by measuring CO2 production from palmitate oxidation relative to total CO2 production.

Main Results:

  • Fatty acid (FA) utilization increased significantly, contributing 48% to overall substrate oxidation in denervated hearts compared to 31% in controls.
  • The ratio of CO2 production from palmitate oxidation to total CO2 production rose from 4.0% in controls to 10.6% in denervated hearts (p=0.04).
  • The time course of FA uptake to CO2 product release remained unchanged, indicating unaltered oxidation kinetics.

Conclusions:

  • Chronic cardiac denervation enhances the contribution of fatty acid (FA) oxidation to myocardial energy metabolism.
  • This metabolic shift is proposed to stem from reduced activity of pyruvate dehydrogenase, likely due to chronic catecholamine depletion.
  • The findings highlight a compensatory metabolic adaptation in the denervated heart towards lipid utilization.
Abstract

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