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J. Lipid Res.
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A more recent version of this article appeared on June 1, 2003

Papers In Press, published online ahead of print April 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300003-JLR200
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Submitted on January 2, 2003
Revised on March 24, 2003
Accepted on April 2, 2003

Increased expression of the SNARE accessory protein Munc18c in lipid-mediated insulin resistance

Isabel R. Schlaepfer, Leslie K. Pulawa, Luis D.M.C-B Ferreira, David E. James, Warren H. Capell, and Robert H. Eckel

Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262

Corresponding Author: Isabel.Schlaepfer{at}UCHSC.edu

Fatty acids inhibit insulin-mediated glucose metabolism in skeletal muscle, an effect largely attributed to defects in insulin-mediated glucose transport. Insulin resistant mice transgenic for the overexpression of LPL in skeletal muscle were used to examine the molecular mechanism(s) in more detail. Using DNA gene chip array technology, and confirmation by RT-PCR and western analysis, increases in the yeast Sec1p homologue Munc18c mRNA and protein were found in the gastrocnemius muscle of transgenic mice, but not other tissues. Munc18c has been previously demonstrated to impair insulin-mediated glucose transport in mammalian cells in vitro. Of interest, stably transfected C2C12 cells overexpressing LPL not only demonstrated increases in Munc18c mRNA and protein but also in transcription rates of the Munc18c gene. To confirm the relevance of fatty acid metabolism and insulin resistance to the expression of Munc18c in vivo, a two-fold increase in Munc18c protein was demonstrated in mice fed a high fat diet for 4 wk. Together, these data are the first to implicate in vivo increases in Munc18c as a potential contributing mechanism to fatty acid-induced insulin resistance.


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