Reduced Adiposity and Liver Steatosis by Stearoyl-CoA Desaturase Deficiency Are Independent of Peroxisome

Stearoyl-CoA desaturase catalyzes the rate-limiting step in the biosynthesis of monounsaturated fatty acids, which are required for normal rates of synthesis of trig-lycerides, cholesterol esters, and phospholipids. Mice with a targeted disruption of the stearoyl-CoA desatu-rase 1 (SCD1) isoform are protected against diet and leptin deficiency-induced adiposity, have increased en-ergy expenditure, and have up-regulated expression of hepatic genes encoding enzymes of fatty acid -oxida-tion. Because peroxisome proliferator-activated recep-tor- (PPAR) is a key transcription factor that induces the transcription of fatty acid -oxidation and thermo-genic genes, we hypothesized that the increased fatty acid oxidation observed in SCD1 deficiency is depend-ent on activation of the PPAR pathway. Here we sho