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Diabetic peripheral neuropathy: role of reactive oxygen and nitrogen species.

Abstract
The prevalence of diabetes has reached epidemic proportions. There are two forms of diabetes: type 1 diabetes mellitus is due to auto-immune-mediated destruction of pancreatic β-cells resulting in absolute insulin deficiency and type 2 diabetes mellitus is due to reduced insulin secretion and or insulin resistance. Both forms of diabetes are characterized by chronic hyperglycemia, leading to the development of diabetic peripheral neuropathy (DPN) and microvascular pathology. DPN is characterized by enhanced or reduced thermal, chemical, and mechanical pain sensitivities. In the long-term, DPN results in peripheral nerve damage and accounts for a substantial number of non-traumatic lower-limb amputations. This review will address the mechanisms, especially the role of reactive oxygen and nitrogen species in the development and progression of DPN.
AuthorsLouis S Premkumar, Reddy M Pabbidi
JournalCell biochemistry and biophysics (Cell Biochem Biophys) Vol. 67 Issue 2 Pg. 373-83 (Nov 2013) ISSN: 1559-0283 [Electronic] United States
PMID23722999 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
Chemical References
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Mitogen-Activated Protein Kinases
Topics
  • Animals
  • Diabetic Neuropathies (complications, metabolism, physiopathology)
  • Humans
  • Hyperglycemia (complications)
  • Mitogen-Activated Protein Kinases (metabolism)
  • Reactive Nitrogen Species (metabolism)
  • Reactive Oxygen Species (metabolism)
  • Sensory Receptor Cells (physiology)

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