title: [Etiopathogenesis of diabetic neuropathy].
abstract: The cause of diabetic neuropathy remains unclear but several mechanisms have been considered. Hyperglycemia with all its metabolic and vascular consequences probably plays the main role. Metabolic consequences of hyperglicemia including increased level of sorbitol and fructose, myoinositol deficiency and Na+/K+ adenosine triphosphate deficiency alter the function of peripheral nerves and lead to an oxidative stress, which changes fatty acid metabolism. Chronic hyperglycemia is also responsible for abnormalities in microcirculation that could lead to local ischemia evoking many endothelial changes. There are also some genetic factors, impaired neurotrophic support and autoimmune damage that influence sensitivity to peripheral nerve damage in diabetes mellitus.
authors.affiliation: Klinika Neurologii Collegium Medicum Uniwersytetu Jagiellońskiego w Krakowie.
authors.forename: E A
authors.initials: EA
authors.lastname: Gryz
authors.forename: D
authors.initials: D
authors.lastname: Galicka-Latała
authors.forename: A
authors.initials: A
authors.lastname: Szczudlik
authors.forename: J
authors.initials: J
authors.lastname: Sieradzki
mesh_terms: D003929:Diabetic Neuropathies / Q000453:epidemiology / Q000209:etiology*; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism; D015994:Incidence; D018384:Oxidative Stress
chemical_list: D005227:Fatty Acids