Context: Polycystic ovary syndrome (PCOS) affects 5-8% of fertile women and is often accompanied by insulin resistance, leading to increased risk of developing type 2 diabetes. Skeletal muscle from insulin-resistant PCOS subjects display reduced expression of nuclear encoded genes involved in mitochondrial oxidative metabolism.
Objective: We aimed to investigate whether there was a primary mitochondrial dysfunction or difference in mitochondria content that might contribute to the in vivo detected insulin resistance.
Design: The ATP synthesis with and without ATP use and the mitochondrial mass was determined in mitochondria isolated from myotubes established from PCOS subjects and control subjects.
Patients: Myotubes were established from eight insulin-resistant PCOS subjects (verified by euglycemic hyperinsulinemic clamp) and eight healthy weight- and age-matched controls.
Results: Mitochondrial mass and measurable mitochondrial ATP synthesis, with and without ATP use, were not different between PCOS subjects and control subjects.
Conclusion: We found no evidence for a primary impaired mitochondrial function or content in myotubes established from PCOS subjects, and our results suggest that reduced expression of oxidative genes in PCOS subjects is an adaptive trait.