In order to adapt to the rapid development of modern life, reduced physical activity and increased energy intake has led to the onset of obesity , and obesity exacerbated diabetes, coronary artery disease, high blood pressure and nonalcoholic fatty liver diseases. The occurrence of these diseases is related to the lipid distribution in the cells, and SCD-1 is proposed as a potential means of treating obesity and metabolic syndrome. The expression level of SCD-1 in obese mouse model is high, which shows the phenotype of liver fat metamorphosis and insulin resistance. Conversely, in the SCD-1-deficient mouse model, it is sensitive to insulin. In addition, high triglyceride is associated with increased activity of SCD1. Further studies have shown that the increase of SCD-activity can inhibit ABCA1-mediated alcohol output, while SCD1 deficiency reduces the synthesis level of VLDL in obese mouse. Also, a large number of studies have confirmed that SCD-1 is the key to lipid homeostasis and weight control, revealing the prospect of SCD-1 as a therapeutic tool for obesity and other metabolic syndromes.