Corticosteroids (glucocorticoid hormones) are used worldwide by at least 1% of the world population to combat inflammation and cancer. A typical corticosteroid-associated weight gain in patients, common with long-term systemic use, has since long been considered only psychologically burdening. However, this side effect is now regarded as potentially dangerous since increased abdominal fat is undoubtedly linked with increased risk of heart disease and type II diabetes. The molecular basis of adipocyte dysfunction, especially in an inflammatory context, is an understudied research topic. In addition, recent reports support that obesity, characterized by imbalances in fat metabolism, is coupled to a chronic low-grade systemic inflammation. Our own work underbuilds that visceral adipocytes, subject to palmitate as a metabolic stressor, exhibit increased expression of cytokines. How anti-inflammatory glucocorticoids lead to an accumulation of visceral fat, which leads to a pro-inflammatory state, is a mechanistically unclear paradox that remains to be solved. Different ligands that trigger the Glucocorticoid Receptor in different ways have been compared for their differential gene regulatory profile in healthy versus metabolically stressed mature human primary adipocyte cells. To provide an explanation for the dysregulated adipocyte functioning upon glucocorticoid treatment we continue in this project with validations of novel hypotheses based on RNA sequencing results.