Boushel 2007 Diabetologia

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Boushel RC, Gnaiger E, Schjerling P, Skovbro M, Kraunsoee R, Dela F (2007) Patients with Type 2 diabetes have normal mitochondrial function in skeletal muscle. Diabetologia 50:790-6.

» PMID: 17334651 Open Access

Boushel RC, Gnaiger E, Schjerling P, Skovbro M, Kraunsoee R, Dela F (2007) Diabetologia

Abstract: Aims/hypothesis: Insulin resistance and type 2 diabetes are associated with mitochondrial dysfunction. The aim of the present study was to test the hypothesis that oxidative phosphorylation and electron transport capacity are diminished in the skeletal muscle of type 2 diabetic subjects, as a result of a reduction in the mitochondrial content. Materials and methods: The O2 flux capacity of permeabilised muscle fibres from biopsies of the quadriceps in healthy subjects (n=8; age 58±2 years [mean±SEM]; BMI 28±1 kg/m2; fasting plasma glucose 5.4±0.2 mmol/l) and patients with type 2 diabetes (n=11; age 62±2 years; BMI 32±2 kg/m2; fasting plasma glucose 9.0±0.8 mmol/l) was measured by high-resolution respirometry.

Results: O2 flux expressed per mg of muscle (fresh weight) during ADP-stimulated state 3 respiration was lower ( p<0.05) in patients with type 2 diabetes in the presence of complex I substrate (glutamate) (31±2 vs 43±3 pmol O2 s-1 mg-1) and in response to glutamate + succinate (parallel electron input from complexes I and II) (63±3 vs 85±6 pmol s-1 mg-1). Further increases in O2 flux capacity were observed in response to uncoupling by FCCP, but were again lower ( p<0.05) in type 2 diabetic patients than in healthy control subjects (86±4 vs 109±8 pmol s-1 mg-1). However, when O2 flux was normalised for mitochondrial DNA content or citrate synthase activity,there were no differences in oxidative phosphorylation or electron transport capacity between patients with type 2 diabetes and healthy control subjects.

Conclusions/interpretation: Mitochondrial function is normal in type 2 diabetes. Blunting of coupled and uncoupled respiration in type 2 diabetic patients can be attributed to lower mitochondrial content.

Keywords: Diabetes, Mitochondria, Skeletal muscle Bioblast editor: Gnaiger E O2k-Network Lab: DK Copenhagen Dela F, AT Innsbruck Gnaiger E, SE Stockholm Boushel RC, CA Vancouver Boushel RC, DK Copenhagen Larsen S

Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Medicine  Pathology: Diabetes, Obesity 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: Coupling efficiency;uncoupling, Substrate  Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k, O2k-Protocol 



SUIT protocol

» SUIT-011


Some concentrations of substrates applied in the respirometric protocols are reported in this publication to have been higher than in MiPNet09.12, but actually the concentrations have been applied according to MiPNet09.12.

MitoEAGLE VO2max/BME data base

  • Human vastus lateralis
  • 8 males
  • 58 years
  • Western sedentary lifestyle, routine activities (walking, gardening..), not engaged in regular structured aerobic or strength training programmes or athletics; non-diabetic controls
  • h = 1.79 m
  • m = 90 kg
  • BME = 1.34
  • BMI = 28.1 kg·m-2
  • VO2max/BM = 31.2 mL·min-1·kg-1
  • Permeabilized muscle fibres; 37 °C; GMSP; mw
  • JO2,P(NS) = 85.4 µmol·s-1·kg-1 wet muscle mass

  • Human vastus lateralis
  • 11 males
  • 62 years
  • T2 Diabetic patients
  • h = 1.77 m
  • m = 100.5 kg
  • BME = 1.55
  • BMI = 32.1 kg·m-2
  • VO2max/BM
  • Permeabilized muscle fibres; 37 °C; GMSP; mw
  • JO2,P(NS) = 63.5 µmol·s-1·kg-1 wet muscle mass