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Mitochondrial oxidative function and type 2 diabetes.

Rasmus Rabøl1, Robert Boushel, Flemming Dela

  • 1The Copenhagen Muscle Research Centre, The Panum Institute, Department of Medical Physiology, University of Copenhagen, Blegdamsvej 3, DK 2200 Copenhagen N, Denmark. rasmusr@mfi.ku.dk

Applied Physiology, Nutrition, and Metabolism = Physiologie Appliquee, Nutrition Et Metabolisme
|January 11, 2007
PubMed
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The exact cause of type 2 diabetes remains unknown, but skeletal muscle mitochondrial function may be impaired. Research indicates reduced oxidative enzyme activity and damaged mitochondria in type 2 diabetics, though functional impairment evidence is not convincing.

Area of Science:

  • Metabolic disorders
  • Mitochondrial function
  • Type 2 diabetes

Background:

  • Insulin resistance and type 2 diabetes causes are unknown.
  • Skeletal muscle is key for glucose disposal.
  • Increased intramyocellular lipids correlate with insulin resistance and reduced mitochondrial oxidative phosphorylation.

Purpose of the Study:

  • Review current knowledge on oxidative enzyme and electron transport chain (ETC) activity in skeletal muscle of type 2 diabetics.
  • Discuss methods for studying mitochondrial function.
  • Explore the link between physical activity and mitochondrial function in type 2 diabetes.

Main Methods:

  • Biochemical assays of oxidative enzymes and ETC activity.
  • Mitochondrial isolation for respiration and ATP production measurements.

Related Experiment Videos

  • Nuclear magnetic resonance (NMR) spectroscopy for indirect ATP production assessment.
  • Analysis of biochemical markers for mitochondrial content.

    • Main Results:

    • Reduced oxidative enzyme activity observed in skeletal muscle of type 2 diabetics, independent of muscle fiber type.
    • Visual evidence of damaged mitochondria accompanies reduced enzyme activity.
    • Decreased mitochondrial content is the primary explanation for reduced oxidative enzyme activity, not convincing evidence of functional impairment.
    • Early metabolic defects in offspring include reduced basal ATP production and attenuated insulin response.

    Conclusions:

    • Evidence for functional mitochondrial impairment in type 2 diabetes is not convincing.
    • Intervention studies correlating insulin resistance and mitochondrial function changes are lacking.
    • The impact of physical activity on mitochondrial function and plasticity in type 2 diabetes requires further research.