Stearoyl-coA desaturase-1 (SCD1) activity has been linked to the development of obesity and the metabolic syndrome (MetS) through its central role in lipid metabolism. Understanding how changes in SCD1 activity affect obesity and MetS risk biomarkers and investigating how these changes in activity affect nutrient handling in non-hepatic tissues is also important. This study investigated how acute SCD1 inhibition effected plasma lipids, skeletal muscle nutrient handling and insulin signaling in mice fed a high-carbohydrate very-low fat diet for 10 weeks. This study demonstrated that SCD1 inhibition created acute dyslipidemia, altered nutrient handling protein activity and increased the percentage of saturated fatty acids (SFA) in hepatic and muscle tissue, independent of dietary oleic acid content. However, the molecular controls of protein synthesis in the mTOR pathway were not affected by the loss of SCD1 activity. In conclusion, we observed that inhibiting hepatic SCD1 activity and subsequently changing the monounsaturated fatty acid (MUFA) to SFA ratios in tissues alters normal nutrient handling in skeletal muscle.

Stearoyl-coA desaturase-1 (SCD1) activity has been linked to the development of obesity and the metabolic syndrome (MetS) through its central role in lipid metabolism. Understanding how changes in SCD1 activity affect obesity and MetS risk biomarkers and investigating how these changes in activity affect nutrient handling in non-hepatic tissues is also important. This study investigated how acute SCD1 inhibition effected plasma lipids, skeletal muscle nutrient handling and insulin signaling in mice fed a high-carbohydrate very-low fat diet for 10 weeks. This study demonstrated that SCD1 inhibition created acute dyslipidemia, altered nutrient handling protein activity and increased the percentage of saturated fatty acids (SFA) in hepatic and muscle tissue, independent of dietary oleic acid content. However, the molecular controls of protein synthesis in the mTOR pathway were not affected by the loss of SCD1 activity. In conclusion, we observed that inhibiting hepatic SCD1 activity and subsequently changing the monounsaturated fatty acid (MUFA) to SFA ratios in tissues alters normal nutrient handling in skeletal muscle.