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.