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J. Biol. Chem., Vol. 282, Issue 4, 2483-2493, January 26, 2007

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Stearoyl-CoA Desaturase-1 Mediates the Pro-lipogenic Effects of Dietary Saturated Fat^*

Harini Sampath, Makoto Miyazaki, Agnieszka Dobrzyn¹, and James M. Ntambi²

From the Departments of Nutritional Sciences and Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Dietary saturated fats have often been implicated in the promotion of obesity and related disorders. It has been shown recently that saturated fats act through the transcription factor SREBP-1c (sterol regulatory element-binding protein-1c) and its requisite coactivator, peroxisome proliferator-activated receptor- coactivator-1 (PGC-1), to exert their pro-lipogenic effects. We show here that a diet high in the saturated fat stearate induces lipogenic genes in wild-type mice, with the induction of the Scd1 (stearoyl-CoA desaturase-1) gene preceding that of other lipogenic genes. However, in Scd1^-/- mice, stearate does not induce lipogenesis, and Srebp-1c and Pgc-1 levels are markedly reduced. Instead, genes of fatty acid oxidation such as Cpt-1 (carnitine palmitoyltransferase-1) as well as Pgc-1 are induced. Mitochondrial fatty acid oxidation is increased, and white adipose tissue and hepatic glycogen stores are depleted in stearate-fed Scd1^-/- mice. Furthermore, AMP-activated protein kinase is also induced by stearate feeding in Scd1^-/- mice. These results indicate that the desaturation of saturated fats such as stearate by SCD is an essential step mediating their induction of lipogenesis. In the absence of SCD1, stearate promotes oxidation, leading to protection from saturated fat-induced obesity. SCD1 thus serves as a molecular switch in the promotion or prevention of lipid-induced disorders brought on by consumption of excess saturated fat.

Received for publication, October 30, 2006 , and in revised form, November 20, 2006.

^* This work was supported by National Institutes of Health Grant NIDDK-R0162388 (to J. M. N.) and American Heart Association Predoctoral Fellowship 0415001Z (to H. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Present address: Dept. of Physiology, Medical University of Bialystok, Mickiewicza 2c, 15-089 Bialystok, Poland.

² To whom correspondence should be addressed: Dept. of Biochemistry, University of Wisconsin, 433, Babcock Dr., Madison, WI 53706. Tel.: 608-265-3700; Fax: 608-265-3272; E-mail: ntambi{at}biochem.wisc.edu.

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