Article ViewAbstractThe Review of Diabetic Studies,2009,6,4,230-236.DOI:10.1900/RDS.2009.6.230Published:February 2010Authors:Natalia Vallianou, Angelos Evangelopoulos, and Pavlos Koutalas Author(s) affiliations:Natalia Vallianou, Angelos Evangelopoulos and Pavlos Koutalas Department of Internal Medicine, Polykliniki General Hospital, 3 Pireos Str., 10552 Athens, Greece. Abstract:Diabetic neuropathy presents a major public health problem. It is defined by the symptoms and signs of peripheral nerve dysfunction in diabetic patients, in whom other causes of neuropathy have been excluded. Pathogenetic mechanisms that have been implicated in diabetic neuropathy are: a) increased flux through the polyol pathway, leading to accumulation of sorbitol, a reduction in myo-inositol, and an associated reduced Na+-K+-ATPase activity, and b) endoneurial microvascular damage and hypoxia due to nitric oxide inactivation by increased oxygen free radical activity. Alpha-lipoic acid seems to delay or reverse peripheral diabetic neuropathy through its multiple antioxidant properties. Treatment with alpha-lipoic acid increases reduced glutathione, an important endogenous antioxidant. In clinical trials, 600 mg alpha-lipoic acid has been shown to improve neuropathic deficits. This review focuses on the relationship of alphalipoic acid and auto-oxidative glycosylation. It discusses the impact of alpha-lipoic acid on hyperglycemia-induced oxidative stress, and examines the role of alpha-lipoic acid in preventing glycation process and nerve hypoxia. Keywords:Advanced glycation end products, Alpha-lipoic acid, Diabetes, Nuclear factorkappaB, Protein kinase C, Reactive oxygen speciesView:RevDiabeticStud-6-4-230.pdf (126.35 KB) PDFClick here to download the PDF file. Images Increased oxidative stress in diabetes appears to be mainly due to hyperglycemia ‹ The Review of Diabetic Studies, Vol. 6, Issue 4, 2009 up Mitochondrial DNA Variants in the Pathogenesis of Type 2 Diabetes - Relevance of Asian Population Studies ›