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How does glucose generate oxidative stress in peripheral nerve?
1Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
International Review of Neurobiology
|August 30, 2002
Summary
Oxidative stress in diabetic peripheral neuropathy is linked to aldose reductase (AR). Both AR inhibitors and antioxidants improve nerve function, suggesting AR
Area of Science:
- Neuroscience
- Endocrinology
- Biochemistry
Background:
- Diabetes-associated oxidative stress impacts the peripheral nervous system, causing nerve deficits.
- Hyperglycemia is a primary driver of oxidative stress in diabetic nerves.
- The roles of hypoxia, metal imbalance, and hyperlipidemia are less established.
Purpose of the Study:
- To investigate the role of oxidative stress in diabetic peripheral neuropathy.
- To examine the involvement of aldose reductase (AR) in oxidative stress and diabetic nerve damage.
- To clarify the mechanisms linking AR, oxidative stress, and neuropathy.
Main Methods:
- Review of in vivo studies on antioxidants and AR inhibitors in diabetic neuropathy models.
- Analysis of the effects of these agents on nerve function, metabolism, and morphology.
- Discussion of potential mechanisms of AR's role in oxidative stress.
Main Results:
- Antioxidants do not inhibit sorbitol pathway activity in vivo.
- Aldose reductase inhibitors and antioxidants show similar beneficial effects on diabetic nerves.
- Evidence suggests AR contributes to oxidative stress and superoxide production in peripheral nerves.
Conclusions:
- Aldose reductase plays a significant role in oxidative stress within the peripheral nerve.
- AR inhibition and antioxidant treatment yield comparable improvements in diabetic neuropathy.
- Further research is needed to elucidate the precise mechanisms of AR's involvement.