Abstract
Dysfunction of pancreatic islet beta cells underlies both type 1 and type 2 diabetes and appears to result in part from the local release of proinflammatory cytokines. An improved understanding of the mechanisms that mediate islet responsiveness to proinflammatory cytokines may therefore expand our knowledge of the role of cytokine signaling in the development of diabetes, providing potential new targets for the development of therapeutics to protect pancreatic islets from inflammation. In this issue of the JCI, Maier and colleagues identify eukaryotic translation initiation factor 5A (eIF5A) as a critical regulator of the inflammatory response in mouse pancreatic islets. I believe these data provide new and important insights into the regulatory pathways that contribute to the development of diabetes and deepen our understanding of the function of the, so far, rather enigmatic cellular protein eIF5A.