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Epidemiology of Diabetes

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Handbook of Epidemiology

Abstract

Diabetes is a heterogeneous group of metabolic diseases that 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 M, Goldstein BJ, van Haeften TW, Lancet 365:1333–1346, 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 JM, Rewers M, Williams R, Zimmet P (eds), The epidemiology of diabetes mellitus: An international perspective, Wiley, Chichester, 2008; Maahs DM, West NA, Lawrence JM, Mayer-Davis EJ, Endocrinol Metab Clin North Am 39:481–497, 2010).

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Schulze, M.B., Hu, F.B. (2022). Epidemiology of Diabetes. In: Ahrens, W., Pigeot, I. (eds) Handbook of Epidemiology. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6625-3_66-1

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