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

V. Schrauwen-Hinderling*, M. Mensink, M.K. Hesselink, J.P. Sels, M.E. Kooi, P. Schrauwen

*Corresponding author for this work

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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/m(2)) 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 micromol/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 (R(2)=0.50, P=0.05), and glucose (R(2)=0.43, p=0.08) levels. Changes in PCr half-time did not correlate with changes in GIR (R(2)=0.08, P=0.49). Conclusion: The rosiglitazone-enhanced insulin sensitivity does not require improved muscular mitochondrial function.
Original languageEnglish
Pages (from-to)2917-2921
JournalJournal of Clinical Endocrinology & Metabolism
Issue number7
Publication statusPublished - 1 Jan 2008

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