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A more recent version of this article appeared on September 1, 2004

Papers In Press, published online ahead of print June 21, 2004
J. Lipid Res., doi:10.1194/jlr.M400039-JLR200
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Submitted on January 30, 2004
Revised on May 17, 2004
Accepted on June 11, 2004

Lack of stearoyl-CoA desaturase 1 upregulates basal thermogenesis, but causes hypothermia in cold environment

Seong-Ho Lee, Agnieszka Dobrzyn, Pawel Dobrzyn, Shaikh M. Rahman, Makoto Miyazaki, and James M. Ntambi

Biochemsitry Dept., University of Wisconsin-Madison, Madison, WI 53706

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

Stearoyl-CoA desaturase (SCD) is a microsomal enzyme involved in the biosynthesis of oleate and palmitoleate. Mice with a targeted disruption of the SCD1 isoform (SCD1-/-) exhibit reduced adiposity and increased energy expenditure. To address whether the energy expenditure is due to increased thermogenesis, we investigated the effect of SCD1 deficiency on basal- and cold-induced thermogenesis. SCD1-/- mice have increased expression of uncoupling proteins (UCP) in brown adipose tissue (BAT) relative to controls. The 3-adrenergic receptor (3-AR) expression was increased and the phosphorylation of cAMP response element binding protein and the protein level of peroxisome proliferator-activated receptor- coactivator-1 were increased in the SCD1-/- mice. Both lipolysis and fatty acid oxidation were increased in the SCD1-/- mice. When exposed to 4°C, SCD1-/- mice showed hypothermia, hypoglycemia and depleted liver glycogen. High levels of dietary oleate partially compensated for the hypothermia and rescued plasma glucose and liver glycogen. The results suggest that SCD1 deficiency stimulates basal thermogenesis through upregulation of the 3-AR-mediated pathway and a subsequent increase in lipolysis and fatty acid oxidation in BAT. The hypothermia and hypoglycemia in cold exposed SCD1-/- mice and compensatory recovery by oleate indicate an important role of SCD1 gene expression in thermoregulation.


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