Jill Lincoln , Hannah R. Shotton
Department of Anatomy and Developmental Biology, University College London, London, UK
Abstract
It has been estimated that up to 50% of patients with type 1 or type 2 diabetes will have the complication of neuropathy. The impact of autonomic neuropathy in diabetes is often underestimated, but it can result in a range of debilitating symptoms including orthostatic hypotension, gastroparesis, disordered gastrointestinal motility, impotence and bladder dysfunction, and it also carries an increased risk of cardiovascular mortality. Reduced blood supply, impaired nerve regeneration, deficient axonal transport, loss of neurotrophic support and metabolic changes induced by hyperglycemia including mitochondrial dysfunction have all been implicated in the development of diabetic neuropathy. Many of these deficits can lead to the production of oxidative stress that appears to be a common factor leading to nerve damage. Studies of animal models have revealed that not all subpopulations of autonomic nerves degenerate in diabetes and that some populations are more difficult to treat once neuropathy has developed. Recent evidence indicates that differences in the level of metabolic activity and in the intrinsic defence mechanisms of subpopulations of autonomic neurons may account for their differential susceptibility to the development of neuropathy in diabetes.
Keywords
Autonomic neuropathy; Diabetes mellitus; Myenteric; Oxidative stress; Sympathetic
