Increased mitochondrial substrate sensitivity in skeletal muscle of patients with type 2 diabetes.
Larsen, S. 1; Stride, N. 1; Hey-Mogensen, M. 1; Hansen, C. N. 1; Andersen, J. L. 2; Madsbad, S. 3; Worm, D. 3; Helge, J. W. 1; Dela, F. 1
[Article]
Diabetologia.
54(6):1427-1436, June 2011.
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Aims/hypothesis: Mitochondrial respiration has been linked to insulin resistance. We studied mitochondrial respiratory capacity and substrate sensitivity in patients with type 2 diabetes (patients), and obese and lean control participants.
Methods: Mitochondrial respiration was measured in permeabilised muscle fibres by respirometry. Protocols for respirometry included titration of substrates for complex I (glutamate), complex II (succinate) and both (octanoyl-carnitine). Myosin heavy chain (MHC) composition, antioxidant capacity (manganese superoxide dismutase [MnSOD]), citrate synthase activity and maximal oxygen uptake (citrate synthase activity and maximal oxygen uptake (VO2max) were also determined. Insulin sensitivity was determined with the isoglycaemic-hyperinsulinaemic clamp technique.
Results: Insulin sensitivity was different (p < 0.05) between the groups (patients
Conclusions/interpretation: Increased mitochondrial substrate sensitivity is seen in skeletal muscle from type 2 diabetic patients and is confined to non-lipid substrates. Respiratory capacity per mitochondrion is not decreased with insulin resistance.
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