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Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes

¹Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark
²Stockholm University College of Physical Education and Sports, GIH, Stockholm, Sweden
³Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
⁴Diabetes Research Centre, Department of Endocrinology, Odense University Hospital, Denmark

Correspondence: k.hojlund{at}dadlnet.dk

We tested the hypothesis of a lower respiratory capacity per mitochondrion in skeletal muscle of type 2 diabetic (T2D) patients compared with obese subjects. Muscle biopsies obtained from 10 obese T2D and 8 obese nondiabetic male subjects were used for assessment of 3-hydroxy-Acyl-CoA-dehydrogenase (HAD) and citrate synthase (CS) activity, uncoupling protein 3 (UCP3) content, oxidative stress measured as 4-hydroxy-2-nonenal (HNE), fiber type distribution and respiration in isolated mitochondria. Respiration was normalized to CS activity (mitochondrial content) in isolated mitochondria. Maximal ADP-stimulated respiration (state 3) with pyruvate+malate and respiration through the electron transport chain (ETC) were reduced in T2D patients, and the proportion of type 2X fibers were higher in T2D patients compared with obese subjects (all P<0.05). There were no differences in respiration with palmitoyl-L-carnitine+malate, CS activity, HAD activity, UCP3 content or oxidative stress measured as HNE between the groups. In the whole group, state 3 respiration with pyruvate+malate and respiration through ETC were negatively associated with HbA1c, and the proportion of type 2X fibers correlated with markers of insulin resistance (P<0.05). In conclusion, we provide evidence for a functional impairment in mitochondrial respiration and increased amount of type 2X fibers in muscle of T2D patients. These alterations may contribute to the development of type 2 diabetes in humans with obesity.

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