Dysfunction of beta cells in the pancreas underlies diabetes onset; this dysfunction is in part initiated by inflammation mediated by cytokines. Previously, there has been a call for more research on the mechanism by which beta cells respond to cytokines if protective therapies were available.
Researchers at the Indiana University School of Medicine have done just this, identifying the role of a particular protein-- eIF5A. By depleting this specific protein, preventing it from becoming active, and blocking its modification to contain hypsusine, mice were protected from developing diabetes. The researchers, under Dr. Raghavendra G. Mirmira, found that eIF5A was involved in the production of pro-inflammatory cytokines that leads to islet dysfunction and thus diabetes onset. They propose that a new form of therapy should capitalize on these mice trials that show that eIF5A depletion and hypusination inhibition protects against glucose intolerance .
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