| abstract |
Pancreatic islet dysfunction, in both type 1 and type 2 diabetes results, in part, from cytokine-mediated inflammation leading to iNOS generation and the death of pancreatic islets. The production of pro-inflammatory cytokines involved in the generation of iNOS is facilitated by the availability of the hypusine-containing translational factor eIF5A, necessary for the maturation of antigen-presenting cells. Treatment with agents capable of interfering with the mRNA translating iNOS or with agents that can interfere with the hypusination of eIF5A, prevents the death of islets, lowers blood glucose levels, avoids insulin resistance, and generally avoids the inflammatory response in islets associated with type 1 and type 2 diabetes. |