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J. Lipid Res.
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A more recent version of this article appeared on December 1, 2006 Originally published In Press as doi:10.1194/jlr.M600203-JLR200 on September 28, 2006 Originally published In Press as doi:10.1194/jlr.M600203-JLR200 on September 27, 2006

Papers In Press, published online ahead of print September 28, 2006
J. Lipid Res., doi:10.1194/jlr.M600203-JLR200
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Submitted on May 10, 2006
Revised on September 7, 2006
Accepted on September 26, 2006

Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet

Matthew T. Flowers, Albert K. Groen, Angie Tebon Oler, Mark P. Keller, YounJeong Choi, Kathryn L. Schueler, Oliver C. Richards, Hong Lan, Makoto Miyazaki, Folkert Kuipers, Christina M. Kendziorski, James M. Ntambi, and Alan D. Attie

Biochemistry, University of WIsconsin-Madison, Madison, WI 53706

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

Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat (VLF) diet, SCD1-/- mice developed severe hypercholesterolemia, characterized by an increase in apoB-containing lipoproteins and the appearance of lipoprotein-X. The rate of LDL clearance was decreased in VLF SCD1-/- mice relative to VLF SCD1+/+ mice, indicating that reduced apoB-containing lipoprotein clearance contributed to the hypercholesterolemia. Additionally, HDL-cholesterol was dramatically reduced in these mice. The presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF SCD1-/- mice is indicative of cholestasis. Supplementation of the VLF diet with MUFA- and PUFA-rich canola oil, but not saturated fat-rich hydrogenated coconut oil, prevented these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing LDL cholesterol, signifying a role for dietary PUFA deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Therefore, endogenous MUFA synthesis is essential during dietary unsaturated fat insufficiency and influences the dietary requirement of PUFA.


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