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Published on: July 14, 2023
Diabetes and the peripheral nerve.
1Pennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, Louisiana 70808, USA. obrosoig@pbrc.edu
Biochimica Et Biophysica Acta
|December 9, 2008
Summary
Peripheral diabetic neuropathy (PDN) arises from diabetes-induced nerve damage. This review details multiple hyperglycemia-driven mechanisms contributing to PDN pathogenesis and its complications.
Area of Science:
- Neuroscience
- Endocrinology
- Metabolic Disorders
Background:
- Peripheral diabetic neuropathy (PDN) is a severe complication of diabetes mellitus, often leading to foot amputation.
- Its development involves complex interactions initiated by hyperglycemia, affecting insulin signaling, inflammation, and metabolism.
Purpose of the Study:
- To review recent experimental and clinical findings on the pathogenesis of peripheral diabetic neuropathy (PDN).
- To highlight key mechanisms contributing to PDN development.
Main Methods:
- Review of experimental data from animal and cell culture models.
- Analysis of clinical data related to PDN.
Main Results:
- Established hyperglycemia-initiated mechanisms include increased aldose reductase activity, non-enzymatic glycation/glycooxidation, and protein kinase C activation.
- Emerging mechanisms involve oxidative-nitrosative stress, poly(ADP-ribose) polymerase activation, MAPK and COX-2 activation, and impaired calcium homeostasis.
Conclusions:
- Multiple interconnected pathways contribute to the development of PDN.
- Understanding these mechanisms is crucial for developing effective treatments for diabetic neuropathy.
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