title: Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function.
abstract: Diabetic polyneuropathy (DPN) is defined as peripheral nerve dysfunction. There are three main alterations involved in the pathologic changes of DPN: inflammation, oxidative stress, and mitochondrial dysfunction. Inflammation induces activation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinases. Oxidative stress induced by hyperglycemia is mediated by several identified pathways: polyol, hexosamine, protein kinase C, advanced glycosylation end-products, and glycolysis. In addition, mitochondrial dysfunction accounts for most of the production of reactive oxygen and nitrosative species. These free radicals cause lipid peroxidation, protein modification, and nucleic acid damage, to finally induce axonal degeneration and segmental demyelination. The prevalence of DPN ranges from 2.4% to 78.8% worldwide, depending on the diagnostic method and the population assessed (hospital-based or outpatients). Risk factors include age, male gender, duration of diabetes, uncontrolled glycaemia, height, overweight and obesity, and insulin treatment. Several diagnostic methods have been developed, and composite scores combined with nerve conduction studies are the most reliable to identify early DPN. Treatment should be directed to improve etiologic factors besides reducing symptoms; several approaches have been evaluated to reduce neuropathic impairments and improve nerve conduction, such as oral antidiabetics, statins, and antioxidants (alpha-lipoic acid, ubiquinone, and flavonoids).
authors.affiliation: Departamento de Ciencias de la Salud-Enfermedad, Centro Universitario de Tonalá, Universidad de Guadalajara, Guadalajara, JAL, Mexico.
authors.forename: Luis Miguel
authors.initials: LM
authors.lastname: Román-Pintos
authors.affiliation: Departamento de Ciencias de la Salud-Enfermedad, Centro Universitario de Tonalá, Universidad de Guadalajara, Guadalajara, JAL, Mexico; Unidad de Investigación Médica, Instituto de Investigación Clínica de Occidente, Guadalajara, JAL, Mexico.
authors.forename: Geannyne
authors.initials: G
authors.lastname: Villegas-Rivera
authors.affiliation: Instituto de Terapéutica Experimental y Clínica, Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, JAL, Mexico.
authors.forename: Adolfo Daniel
authors.initials: AD
authors.lastname: Rodríguez-Carrizalez
authors.affiliation: Instituto de Terapéutica Experimental y Clínica, Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, JAL, Mexico.
authors.forename: Alejandra Guillermina
authors.identifier: 0000-0002-3635-6135
authors.initials: AG
authors.lastname: Miranda-Díaz
authors.affiliation: Instituto de Terapéutica Experimental y Clínica, Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, JAL, Mexico.
authors.forename: Ernesto Germán
authors.initials: EG
authors.lastname: Cardona-Muñoz
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000378:metabolism*; D003929:Diabetic Neuropathies / Q000453:epidemiology / Q000378:metabolism*; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D007328:Insulin / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D015995:Prevalence; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D005609:Free Radicals; D007328:Insulin; D017382:Reactive Oxygen Species