Format

Send to

Choose Destination
Eur J Pharmacol. 1999 Jun 30;375(1-3):217-23.

Glucose-induced oxidative stress and programmed cell death in diabetic neuropathy.

Author information

1
Department of Internal Medicine, and Michigan Diabetes Research and Training Center, University of Michigan, Ann Arbor, USA. dgreene@umich.edu

Abstract

The Diabetes Control and Complications Trial (DCCT) established the importance of hyperglyemia and other consequences of insulin deficiency in the pathogenesis of diabetic neuropathy, but the precise mechanisms by which metabolic alterations produce peripheral nerve fiber damage and loss remain unclear. Emerging data from human and animal studies suggest that glucose-derived oxidative stress may play a central role, linking together many of the other currently invoked pathogenetic mechanisms such as the aldose reductase and glycation pathways, vascular dysfunction, and impaired neurotrophic support. These relationships suggest combinations of pharmacological interventions that may synergistically protect the peripheral nervous system (PNS) against the metabolic derangements of diabetes mellitus.

PMID:
10443578
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center