Stearoyl-CoA desaturase-1 activity in skeletal muscle: Is it good or bad?

Abstract

Skeletal muscle is known to be an important site for metabolic processes such as glucose disposal and fatty acid oxidation, and, as such, dysregulation of these processes in muscle is associated with and may play a causative role in many disease states and comorbidities including obesity, hypertension, insulin resistance, and hypertriglyceridemia (Lee et al. 2003; McGarry 2002; Petersen and Shulman 2002; Scheuermann-Freestone et al. 2003). Specifically, these disease/co-morbid states are associated with dysregulated glucose and fatty acid metabolism and excess lipid accumulation in skeletal muscle (Flowers and Ntambi 2009; Kahn and Flier 2000). Studies in humans show that SCD1 is associated with insulin resistance, increased intramuscular triacylglycerol (IMTG) content, and reduced fatty acid oxidation (Dubé et al. 2011; Hulver et al. 2005). Studies in rodents clearly show that genetic deletion of SCD1 prevents high-fat diet-induced weight gain and insulin resistance (Ntambi et al. 2002). Conversely, others have suggested that heightened SCD1 activity in skeletal muscle may be protective (Dobrzyn et al. 2010; Schenk and Horowitz 2007). To date, the role of SCD1 in dysregulated metabolism, specifically in skeletal muscle, is not definitively known, as there are conflicting reports. The purpose of this chapter is to highlight the available evidence for both the deleterious and protective roles of SCD1 in the context of metabolic deranged states such as insulin resistance and obesity. The role of SCD1 in the context of inflammatory signaling and adaptation to exercise will also be touched upon.