Abstract
All forms of diabetes are characterized by hyperglycemia, a relative or absolute lack of insulin action, and the development of diabetes-specific pathology in the retina, renal glomerulus, and peripheral nerve. Diabetes is also associated with accelerated atherosclerotic disease, which affects arteries that supply the heart, brain, and lower extremities. As a consequence of its disease-specific pathology, in the developed world diabetes mellitus is now the leading cause of new blindness in working-age people and the leading cause of end-stage renal disease (ESRD). More than 60% of diabetic patients are affected by neuropathy, which includes distal symmetrical polyneuropathy (DSPN), mononeuropathies, and a variety of autonomic neuropathies that cause erectile dysfunction, urinary incontinence, gastroparesis, and nocturnal diarrhea. Diabetic accelerated lower extremity arterial disease in conjunction with neuropathy accounts for more than 50% of all nontraumatic amputations in the USA [1].
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Giacco, F., Brownlee, M. (2012). Mechanisms of Hyperglycemic Damage in Diabetes. In: Skyler, J. (eds) Atlas of Diabetes. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-1028-7_10
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DOI: https://doi.org/10.1007/978-1-4614-1028-7_10
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