期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 121, 期 6, 页码 2457-2461出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI46405
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资金
- Wellcome Trust
- UK National Institute for Health Research Cambridge Biomedical Research Centre
- UK Medical Research Council Centre for Obesity and Related Metabolic Diseases
- Clinical Research Infrastructure Grant
- MRC [G0701532, MC_U106179473] Funding Source: UKRI
- Medical Research Council [G0701532, MC_U106179473, G0600717B] Funding Source: researchfish
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.
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