Lack of stearoyl-CoA desaturase-1 function induces a palmitoyl-CoA Δ6 desaturase and represses the stearoyl-CoA desaturase-3 gene in the preputial glands of the mouse

• Published in: Journal of lipid research 2002-12, Vol.43 (12), p.2146-2154
• Main Authors: Miyazaki, Makoto, Gomez, Francisco Enrique, Ntambi, James M.
• Format: Article
• Language: English
• Subjects: gene isoforms; triglycerides; wax esters; Δ6 hexadecenoic acid
• ISSN: 0022-2275
• DOI: 10.1194/jlr.M200271-JLR200

The mouse preputial gland (222298), 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 Δ9 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 (Δ6 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 Δ6 desaturase activity. Testosterone administration to the SCD1−/− mouse induced SCD3 mRNA expression and resulted in an increase in the Δ9 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 Δ6 desaturase enzyme in mammals.