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This version published online on May 6, 2008
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2008-0267
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Submitted on February 5, 2008
Accepted on April 29, 2008

The insulin sensitizing effect of rosiglitazone in type 2 diabetes mellitus patients does not require improved in vivo muscle mitochondrial function

Vera B. Schrauwen-Hinderling (PhD)*, Marco Mensink (MD, PhD), Matthijs K.C. Hesselink (PhD), Jean-Pierre Sels (MD, PhD), Marianne Eline Kooi (PhD), and Patrick Schrauwen (PhD)

Departments of Radiology, and Internal Medicine, Maastricht University Hospital, The Netherlands; Nutrition and Toxicology Research Institute Maastricht, NUTRIM, Maastricht University, The Netherlands; Departments of Human Biology, and Human Movement Sciences, Maastricht University, The Netherlands

* To whom correspondence should be addressed. E-mail: v.schrauwen{at}hb.unimaas.nl.

Aims: To investigate whether improved in vivo mitochondrial function in skeletal muscle and intramyocellular lipids (IMCL) contribute to the insulin-sensitizing effect of rosiglitazone.

Methods: Eight overweight type 2 diabetic patients (BMI= 29.3 ± 1.1 kg/m2) were treated with rosiglitazone for 8 weeks. Before and after treatment, insulin sensitivity was determined by a hyperinsulinaemic-euglycaemic clamp. Muscular mitochondrial function (half-time of phosphocreatine recovery after exercise) and IMCL content were measured by magnetic resonance spectroscopy.

Results: Insulin sensitivity improved after rosiglitazone (GIR: 19.9±2.8 to 24.8±2.1 µmol/kg/min (P<0.05)). In vivo mitochondrial function (PCr recovery half-time: 23.8±3.5 to 20.0±1.7 s (P=0.23)) and IMCL content (0.93±0.18% to 1.37±0.40%, p=0.34) did not change. Interestingly, the changes in PCr half-time correlated/tended to correlate with changes in fasting insulin (R2=0.50, P=0.05), and glucose (R2=0.43, p=0.08) levels. Changes in PCr half-time did not correlate with changes in GIR (R2=0.08, P=0.49).

Conclusion: The rosiglitazone-enhanced insulin sensitivity does not require improved muscular mitochondrial function.






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