Mitochondrial dysfunction is associated with insulin resistance and type 2 diabetes. It has thus been suggested that primary and/or genetic abnormalities in mitochondrial function may lead to accumulation of toxic lipid species in muscle and elsewhere, impairing insulin action on glucose metabolism. Alternatively, however, defects in insulin signaling may be primary events that result in mitochondrial dysfunction, or there may be a bidirectional relationship between these phenomena. To investigate this, we examined mitochondrial function in patients with genetic defects in insulin receptor (INSR) signaling. We found that phosphocreatine recovery after exercise, a measure of skeletal muscle mitochondrial function in vivo, was significantly slowed in patients with INSR mutations compared with that in healthy age-, fitness-, and BMI-matched controls. These findings suggest that defective insulin signaling may promote mitochondrial dysfunction. Furthermore, consistent with previous studies of mouse models of mitochondrial dysfunction, basal and sleeping metabolic rates were both significantly increased in genetically insulin-resistant patients, perhaps because mitochondrial dysfunction necessitates increased nutrient oxidation in order to maintain cellular energy levels.

Direct Link: https://doi.org/10.1172/JCI46405

Journal: The Journal of clinical investigation. 2011 Jun 1;121(6):2457-61

Keywords: diabetes, energy expenditure, insulin resistance, mitochondrial dysfunction, phosphocreatine recovery,

Applications: Energy Expenditure,

CamNtech Reference: AH11048

Back to Search Results

UK & International customers

CamNtech Ltd.
Manor Farm
Fenstanton
Cambridgeshire
PE28 9JD, UK

US customers

CamNtech Inc.
630 Boerne Stage Airfield,
Boerne,
Texas 78006,
USA

Copyright

© 2020 CamNtech Ltd and CamNtech Inc

Company information

Registered in England No. 2221302
VAT No: GB486 3019 34


Privacy Policy