Beta-cell failure is central to the pathogenenis of both type 1 and type 2 diabetes mellitus. In type 1 diabetes immune-mediated beta-cell destruction takes place, whereas in type 2 diabetes metabolic factors are believed to induce progressively deteriation of beta-cell function and finally reduced beta-cell mass. The proinflammatory cytokine interleukin-1 could be a mediator of the beta-cell failure in both diseases: In type 1 diabetes by the secretion from actived macrophages inflitrating the islets, and in type 2 diabetes by glucose induced secretion from the beta-cell ifselves. Using the interleukin-1-receptor antagonist in patients with type 2 diabetes improves glycemic control and beta-cell function and reduces markes of systemic inflammation, indicating that type 2 diabetes could be an auto-inflammatory condition. Furthermore the involvement of interferon-gamma and tumor necrosis factor alpha in the pathogenesis of type 1 and type 2 diabetes is reveiwed.
25 - 29 Apr 2009
European Society of Endocrinology