Abstract
Insulin-dependent (type 1) diabetes mellitus (IDDM) is caused by a progressive destruction of insulin-producing β cells in the pancreatic islets of Langerhans.1 Destruction of β cells appears to be mediated by a cell selective autoimmune reactivity which can be triggered by environmental factors in genetically predisposed individuals,2 leading to a life-long dependence on insulin therapy. Despite current modes of treatment, IDDM patients experience episodes of abnormally high blood glucose levels.3 These recurrent hyperglycemia episodes have been suggested to cause the development of chronic lesions which can result in renal failure, blindness, heart disease, neuropathy, and atherosclerosis.4 In recent years a predominant focus of diabetes research has been to attempt and develop new forms of treatment which prevent the disabling neurovascular complications of the disease. Recently, through tight control of blood glucose levels, the Diabetes Control and Complications Trial demonstrated that long-term intensive insulin treatment was associated with a reduction in the risk of developing diabetes-related complications.5 However, this therapy can result in harmful side effects due to hypoglycemia and may be difficult to achieve in all IDDM patients.5 Furthermore, the intensive involvement required for monitoring and providing therapy for these patients may exceed the capabilities of many individuals and their health care providers. An attractive alternative is to transplant insulin-producing tissue, which can offer a more physiological approach for precise restoration of glucose homeostasis, thereby reversing the metabolic and neurovascular complications of diabetes.
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Korbutt, G.S., Warlock, G.L., Rajotte, R.V. (1997). Islet Transplantation. In: Soria, B. (eds) Physiology and Pathophysiology of the Islets of Langerhans. Advances in Experimental Medicine and Biology, vol 426. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1819-2_53
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