Abstract
Background
Insulin is a multifunctional hormone. It provides a link for the regulation of metabolic as well as nonmetabolic cells. Inefficient signal transduction (ie, insulin resistance) is the central pathomechanism in type 2 diabetes mellitus; it also drives atherosclerosis through induction of endothelial dysfunction.
Objective
Because epidermal homeostasis depends on insulin, too, we speculate on a potential role of insulin resistance in the formation of psoriatic plaques.
Methods
We comment on the effects of insulin on keratinocyte biology, with an emphasis on cytokine-induced insulin resistance in the light of recent original work from our group.
Results
There is increasing evidence for cytokine-induced insulin resistance in keratinocytes that contributes to the epidermal phenotype in lesional psoriatic skin.
Conclusion
Pro-inflammatory cytokines might induce a state of epidermal dysfunction, much like the state of endothelial dysfunction induced by similar mechanisms. Kinases involved in insulin- and cytokine-receptor signalling represent potential targets for innovative topical antipsoriatic therapies.
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