White adipose tissue (WAT) has important dual energy-storage and endocrine functions, which become deranged in obesity, contributing to the pathogenesis of inflammatory metabolic disorders such as type-2 diabetes. Humans express SCD1 in WAT, and rodents express both SCD1 and SCD2 in this tissue. WAT SCD expression is regulated by hormones, cytokines, and nutritional status. Leptin, estrogen, and tumor necrosis factor-alpha reduce its expression, while insulin and ghrelin increase it. In humans, hypercaloric or high-carbohydrate diets stimulate WAT SCD expression, while caloric restriction suppresses it. Fatty acids have differential effects on WAT SCD expression with polyunsaturated fatty acids (PUFAs) having an inhibitory effect and saturated fatty acids (SFAs) having a stimulatory effect. Interestingly, effects of peroxisome proliferator-activated receptor gamma agonists are species-specific. WAT SCD plays an important role in modulating metabolic functions. Its expression positively correlates with body weight and insulin resistance. Although germline SCD1 deletion protects mice from diet-induced obesity and insulin resistance, adipose-specific SCD knockout does not provide these protective effects. Therefore, it is likely that WAT SCD upregulation in obesity is an adaption to increased availability of carbohydrates and SFAs. However, since palmitoleate and oleate, two major products of the desaturation reaction catalyzed by this enzyme, regulate inflammatory responses, WAT SCD also appears to be important in modulating adipose tissue inflammation in obesity. In conclusion, SCD is an important enzyme for triglyceride storage of WAT, which has additional functions in regulating metabolism and inflammation, especially in conditions of expanded fat mass.