Patients with type 2 diabetes have normal mitochondrial function in skeletal muscleReport as inadecuate




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Diabetologia

, Volume 50, Issue 4, pp 790–796

First Online: 15 February 2007Received: 11 October 2006Accepted: 17 November 2006

Abstract

Aims-hypothesisInsulin 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 methodsThe 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-m; 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-m; fasting plasma glucose 9.0 ± 0.8 mmol-l was measured by high-resolution respirometry.

ResultsO2 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 mg and in response to glutamate + succinate parallel electron input from complexes I and II 63 ± 3 vs 85 ± 6 pmol s mg. 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 mg. 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-interpretationMitochondrial 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.

KeywordsDiabetes Mitochondria Skeletal muscle AbbreviationsFCCPcarbonylcyanide-4-trifluoromethoxy-phenylhydrazone

mtDNAmitochondrial DNA

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Author: R. Boushel - E. Gnaiger - P. Schjerling - M. Skovbro - R. Kraunsøe - F. Dela

Source: https://link.springer.com/







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