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A more recent version of this article appeared on December 1, 2002

Papers In Press, published online ahead of print September 16, 2002
J. Lipid Res., doi:10.1194/jlr.M200271-JLR200
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Submitted on July 15, 2002
Revised on September 16, 2002
Accepted on September 5, 2002

Lack of stearoyl-CoA desaturase-1 function induces a palmitoyl-CoA D6 desaturase and represses the stearoyl-CoA desaturase-3 gene in the preputial glands of the mouse

Makoto Miyazaki, Fransisco Enrique Gomez, and James M. Ntambi

Biochemistry, University of Wisconsin-Madison, Madison, WI 53706-1554

Corresponding Author: ntambi{at}biochem.wisc.edu

The mouse preputial gland (PG), a specialized sebaceous structure, is rich in wax esters, triglycerides and alkyl-2,3-diacylglycerol. We have found that the mouse PG expresses the three gene isoforms (SCD1, SCD2 and SCD3) of the D9 stearoyl-CoA desaturase enzyme that catalyzes the biosynthesis of monounsaturated fatty acids mainly, C16:1n-7 and C18:1n-9. However, mice with a targeted disruption in the SCD1 isoform (SCD1-/-) have undetectable SCD3 mRNA expression in the PG while the expression of SCD2 isoform was not altered. The levels of C16:1n-7 were reduced by greater than 70% while that of C18:1n-9 were reduced by 28%. The content of the C16:1n-10 (D6 hexadecenoic acid) isomer and a major fatty acid of the PG was increased by greater than 2-fold mainly in the wax ester fraction of the SCD1-/- mouse. We demonstrate that the increase in C16:1n-10 is due to induction of a specific palmitoyl-CoA D6 desaturase activity. Testosterone administration to the SCD1-/- mouse induced SCD3 mRNA expression and resulted in an increase in the D9 desaturation of 16:0-CoA but not of 18:0-CoA. These observations demonstrate that loss of SCD1 function alters the expression of SCD3 and reveal for the first time the presence and regulation of a palmitoyl-CoA D6 desaturase enzyme in mammals


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