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© Cambridge University Press 2007 and Cambridge University Press, 2009. Introduction Type 2 diabetes accounts for the overwhelming majority of diabetes worldwide (Zimmet et al., 2001) and represents a major and growing challenge to biomedical care. In contrast to many other complex traits, the environmental exposures which contribute to the development of this condition are well characterized: but as they are so pervasive, efforts to reduce the prevalence of this condition through environmental and behavioral manipulation have had only limited impact. Personal risk of developing type 2 diabetes results from the interaction between these pervasive exposures and our individual portfolios of susceptibility and protective genomic variants. Over the past decade, more and more of these variants have been identified and characterized. The challenge for the next decade is to understand how these variants interact with each other and with environment, and to use this information to target preventive and therapeutic interventions to maximize their effect. Type 2 diabetes: the next global epidemic? Definitions In contrast to type 1 diabetes, which is known to result from autoimmune destruction of the insulin-secreting beta-cells of the pancreas, leading to lifelong dependence on exogenous insulin, the etiology of type 2 diabetes is poorly understood (Kahn, 2003). Whilst type 1 diabetes is typically diagnosed in childhood or early adulthood, type 2 diabetes classically presents in later life. These clinical distinctions lie behind previous disease classifications in which type 2 diabetes was known originally as maturity-onset diabetes, and subsequently, as non-insulin-dependent diabetes mellitus (World Health Organization Study Group, 1985).

Original publication

DOI

10.1017/CBO9780511543555.024

Type

Chapter

Book title

Genes and Common Diseases

Publication Date

01/01/2007

Pages

344 - 358