Abstract
Diabetes is a heterogeneous group of metabolic diseases which share a common characteristic: hyperglycemia. Hyperglycemia develops as a result of various defects in insulin secretion by pancreatic beta-cells or from changes in insulin action. Either defect jeopardizes the delicate interplay between insulin secretion and insulin action which is essential for the maintenance of normoglycemia. Normal pancreatic beta-cells can adapt to changes in insulin action. For example, under regular circumstances, a decrease in insulin sensitivity in target organs such as muscle is compensated by upregulation of insulin secretion and, alternatively, a decrease in secretory function of beta-cells can be counterbalanced by increases in insulin sensitivity. This hyperbolic relationship between insulin secretion and insulin action is deteriorated in patients with diabetes, resulting in chronically higher than normal levels of glycemia (Stumvoll et al. 2005). Type 2 diabetes, the most common form of diabetes, is characterized by a relative loss of beta-cell function which leads to insufficient compensation for increased insulin resistance. Type 1 diabetes is characterized by an absolute deficiency of insulin secretion resulting from autoimmune destruction of pancreatic beta-cells. Due to the different pathophysiology and causative factors involved, a detailed description of the epidemiology of type 1 diabetes is beyond this chapter. Interested readers should refer to previous reviews (Ekoé et al. 2008; Maahs et al. 2010).
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Schulze, M.B., Hu, F.B. (2014). Epidemiology of Diabetes. In: Ahrens, W., Pigeot, I. (eds) Handbook of Epidemiology. Springer, New York, NY. https://doi.org/10.1007/978-0-387-09834-0_66
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