Diabetes mellitus in childhood: facts and controversies

Abstract

We are in the midst of a diabetes pandemic. In 2000, 171 million people worldwide were affected by the disease with projections that it will affect 366 million by 2030. The incidence of type 1 a diabetes has been doubling approximately every two decades. Perhaps the most striking change in diabetes over recent years has been the convergence of previously distinctive phenotypes. The possibility that type 1 and type 2 diabetes are merely poles of a single spectrum, where variation in the tempo of beta cell loss is determined by age at onset and symptoms at presentation, has important implications. Beta cell deficiency underlies both type 1 and type 2 diabetes, and restoration or replacement of beta cell function is therefore the logical long-term solution to therapy. New beta cells derived from embryonic stem cells may be an interesting future strategy for the treatment of diabetes, but this approach appears to be far from ready for clinical application. "The accelerator hypothesis" proposes that insulin resistance remains the driver responsible for acceleration of beta cell loss among those with reactive immunoresponse genes. Children who develop type 1 diabetes are taller and heavier than their peers. The consequence of more rapid growth is insulin resistance, when beta cells become more active and more antigenic for the immune system. Although immunomodulatory therapy slows the tempo of beta cell loss, insulin resensitization may be an intervention that is more physiological, less toxic and considerably cheaper and would encourage a lifestyle change in the prevention of childhood diabetes.