Stearoyl CoA desaturase 1: role in cellular inflammation and stress

Abstract

Stearoyl CoA desaturase 1 (SCD1) catalyzes the rate-limiting step in the production of MUFA that are major components of tissue lipids. Alteration in SCD1 expression changes the fatty acid profile of these lipids and produces diverse effects on cellular function. High SCD1 expression is correlated with metabolic diseases such as obesity and insulin resistance, whereas low levels are protective against these metabolic disturbances. However, SCD1 is also involved in the regulation of inflammation and stress in distinct cell types, including β-cells, adipocytes, macrophages, endothelial cells, and myocytes. Furthermore, complete loss of SCD1 expression has been implicated in liver dysfunction and several inflammatory diseases such as dermatitis, atherosclerosis, and intestinal colitis. Thus, normal cellular function requires the expression of SCD1 to be tightly controlled. This review summarizes the current understanding of the role of SCD1 in modulating inflammation and stress.

Figure 1

Role of SCD in pathological processes. SCD1 mediates the synthesis of MUFA from dietary or endogenously synthesized SFA. Loss of SCD1 results in a favorable metabolic profile, including an increase in insulin sensitivity and a decrease in hepatic steatosis and adiposity. Inhibition of SCD1 is also associated with a reduction in cancer cell growth. Additionally, suppression of SCD1 alters cellular function by modulating inflammation and stress in a number of cell types and tissues, such as adipocytes, liver, macrophages, aorta, skin, myocyte, β-cell, and endothelial cell. The asterisk denotes mixed observation in a tissue or cell type.