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Diabetes 50:2585-2590, 2001
© 2001 by the American Diabetes Association, Inc.

In Muscle-Specific Lipoprotein Lipase-Overexpressing Mice, Muscle Triglyceride Content Is Increased Without Inhibition of Insulin-Stimulated Whole-Body and Muscle-Specific Glucose Uptake

Peter J. Voshol1,2, Miek C. Jong1, Vivian E.H. Dahlmans1, Dagmar Kratky3, Sanja Levak-Frank4, Rudolf Zechner3, Johannes A. Romijn2, and Louis M. Havekes1,2

1 TNO-Prevention and Health, Division VBO, Leiden, the Netherlands
2 Department of Endocrinology and Metabolic Diseases, Leiden University Medical Centre, Leiden, the Netherlands
3 Institute of Molecular Biology, Biochemistry, and Microbiology, University of Graz, Graz, Austria
4 Institute of Medical Biochemistry and Medical Molecular Biology, University of Graz, Graz, Austria

In patients with type 2 diabetes, a strong correlation between accumulation of intramuscular triclycerides (TGs) and insulin resistance has been found. The aim of the present study was to determine whether there is a causal relation between intramuscular TG accumulation and insulin sensitivity. Therefore, in mice with muscle-specific overexpression of human lipoprotein lipase (LPL) and control mice, muscle TG content was measured in combination with glucose uptake in vivo, under hyperinsulinemic-euglycemic conditions. Overexpression of LPL in muscle resulted in accumulation of TGs in skeletal muscle (85.5 ± 33.3 vs. 25.7 ± 23.1 µmol/g tissue in LPL and control mice, respectively; P < 0.05). During the hyperinsulinemic clamp study, there were no differences in plasma glucose, insulin, and FFA concentrations between the two groups. Moreover, whole-body, as well as skeletal muscle, insulin-mediated glucose uptake did not differ between LPL-overexpressing and wild-type mice. Surprisingly, whole-body glucose oxidation was decreased by ~60% (P < 0.05), whereas nonoxidative glucose disposal was increased by ~50% (P < 0.05) in LPL-overexpressing versus control mice. In conclusion, overexpression of human LPL in muscle increases intramuscular TG accumulation, but does not affect whole-body or muscle-specific insulin-mediated uptake, findings that argue against a simple causal relation between intramuscular TG content and insulin resistance.


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Copyright © 2001 by the American Diabetes Association.