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).
Under the most recent classification of diabetes subtypes, published in 1997 by a joint expert committee of the American Diabetes Association and the World Health Organization, individuals whose diabetes has an established basis - be that causal genetic variation (as in some monogenic forms of diabetes (see below)) or discrete environment risk factors (e.g. certain drugs and poisons) -are excluded from the ''type 2 diabetes'' label, even if there is considerable clinical overlap (The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). There is, however, much to be learned about the molecular basis of type 2 diabetes in general from these rarer instances of known etiology. For the purposes of this chapter, therefore, the term ''type 2 diabetes'' (T2D) is used in a broad sense to include these other, related, types of diabetes.
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