Mitochondrial oxidative stress, mitochondrial dysfunction, or both have been implicated in
insulin resistance. However, disentangling the individual roles of these processes in insulin
resistance has been difficult because they often occur in tandem, and tools that selectively
increase oxidant production without impairing mitochondrial respiration have been lacking.
Using the dimer/monomer status of peroxiredoxin isoforms as an indicator of compartmental
hydrogen peroxide burden, we provide evidence that oxidative stress is localized to …