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A high fat diet increases mitochondrial fatty acid oxidation and uncoupling to decrease efficiency in rat heart.

Mark A Cole1, Andrew J Murray, Lowri E Cochlin

  • 1Department of Physiology, Anatomy and Genetics, University of Oxford, UK. mark.cole@dpag.ox.ac.uk

Basic Research in Cardiology
|February 15, 2011
PubMed
Summary
This summary is machine-generated.

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High-fat diets decrease cardiac efficiency in non-obese rats by increasing oxygen consumption. This is linked to elevated cardiac mitochondrial uncoupling protein 3 (UCP3) and mitochondrial thioesterase 1 (MTE-1) levels.

Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Metabolic Disease

Background:

  • Obesity and diabetes are linked to impaired cardiac function and reduced efficiency.
  • Cardiac mitochondrial uncoupling protein 3 (UCP3) is implicated in these changes in genetic models.

Purpose of the Study:

  • To investigate if cardiac mitochondrial uncoupling occurs in non-genetic obesity induced by a high-fat diet.
  • To determine the impact of a high-fat diet on cardiac function, efficiency, and mitochondrial properties in rats.

Main Methods:

  • Rats were fed either a high-fat diet or standard chow for 3 weeks.
  • Cardiac function was assessed in vivo using cine MRI.
  • Cardiac efficiency, mitochondrial respiration, ADP/O ratios, enzyme activities (MCAD, citrate synthase), and protein levels (UCP3, MTE-1, ANT, ATP synthase) were measured.

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Main Results:

  • High-fat diet consumption led to increased cardiac oxygen consumption (19%) and decreased efficiency (21%) without altering in vivo cardiac function.
  • Mitochondrial fatty acid oxidation and medium chain acyl-CoA dehydrogenase (MCAD) activity were elevated in high-fat-fed rats.
  • Increased respiratory uncoupling, indicated by lower ADP/O ratios, was observed and ameliorated by a UCP3 inhibitor.
  • Levels of cardiac mitochondrial uncoupling protein 3 (UCP3) and mitochondrial thioesterase 1 (MTE-1) were significantly increased.

Conclusions:

  • Non-genetic obesity induced by a high-fat diet reduces cardiac efficiency through increased oxygen utilization.
  • Elevated UCP3 and MTE-1 levels in cardiac mitochondria contribute to increased uncoupling and reduced efficiency.
  • These findings highlight mitochondrial adaptations in the non-obese heart under high-fat conditions.