Introduction It has been reported that insulin resistance is associated with mitochondrial dysfunction in several tissues. While mitochondria are considered central to altered metabolic pathways, leading to pathogenic processes in type 2 diabetes, the mechanisms by which mitochondrial function contributes to the disease remain to be elucidated. Whether it is insulin resistance per se, chronic hyperglycaemia, or accumulation of intracellular lipid and associated alterations in metabolic pathways that affect mitochondrial function, or vice versa, is also unclear. 1 4 3 5 2 1 6 7 8 9 6 2 Subjects and methods Subjects n n 1 1 Table 1 Characteristics of the subjects   n n Age (years) 62 ± 2 58 ± 1 Height (cm) 177 ± 3 179 ± 1 2 32 ± 2* 28 ± 1 Time since diagnosis (years) 5 ± 2 – Fasting insulin (pmol/l) 61 ± 9* 34 ± 6 Fasting glucose (mmol/l) 9.0 ± 0.5* 5.4 ± 0.1 −1 −1 50.8 ± 6.0 58.3 ± 4.7  −1 −1 1.6 ± 0.1 2.0 ± 0.2 3 119 ± 7* 147 ± 12 mtDNA/genomic DNA 2,773 ± 252 3,030 ± 185 p Fig. 1 a b t p Black and white symbols  t 2+ + 2 10 2 2 2 4 −1 −1 2 2 2 2 11 2 Analysis of muscle tissue 12 C t Respirometry protocol c 2 Data analysis t Results p 2 2 2 2 p 2 −1 −1 p 2 2 c 2 Fig. 2 2 2 a b p Black and white bars  1 2 2 2 2 2 3 Fig. 3 a 2 b 2 2  2 1 2 2 1 p 2 r 2 Discussion 2 2 7 8 13 2 2 2 2 V 2max 2 2 2 V 2max 1 14 15 2 16 19 20 21 22 25 26 27 31 32 33 c 34 c V 2max 35 2 3 36 2 3 In conclusion, the results of the present study provide the first direct evidence of normal mitochondrial function in the skeletal muscle of type 2 diabetic subjects. An apparent impairment of oxidative phosphorylation and electron transport capacity is fully accounted for by a diminished mitochondrial content in the diabetic muscle.