Abstract

Glucocorticoids (GC) are potent anti-inflammatory drugs which are widely used in steroid therapy for autoimmune diseases. But besides their beneficial effects, long term treatment induces insulin resistance leading to type 2 diabetes. Until now, the precise molecular mechanisms how GCs induce insulin resistance are ill-defined. GCs act via the glucocorticoid receptor (GR) that can alter gene expression via two different modes of action: either by protein-protein interaction of the monomeric GR with transcription factors such as AP-1 and NF-κB or by direct binding as a homodimer to glucocorticoid response elements (GREs) in the promoter region of target genes. Traditionally GRE induced expression of gluconeogenetic enzymes in the liver by the GR was assumed to be responsible for insulin resistance due to excessive gluconeogenesis.

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