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Diabetic peripheral neuropathy: evidence for apoptosis and associated mitochondrial dysfunction
S Srinivasan1, M Stevens, J W Wiley
1Department of Internal Medicine, University of Michigan, and Ann Arbor VA Medical Centers, USA.
Diabetes
|November 15, 2000
Summary
Diabetic sensory neuropathy involves increased apoptosis and mitochondrial dysfunction in nerve cells. Restoring normal blood sugar levels reversed these harmful effects, suggesting a pathway for treatment.
Area of Science:
- Neuroscience
- Cell Biology
- Metabolic Disorders
Background:
- Diabetic sensory neuropathy is a common complication of diabetes.
- Its underlying mechanisms, particularly the role of apoptosis and mitochondrial dysfunction, require further elucidation.
Purpose of the Study:
- To investigate the association between diabetic sensory neuropathy, apoptosis, and mitochondrial dysfunction in dorsal root ganglion (DRG) neurons.
- To determine the effects of euglycemia restoration on these cellular processes.
Main Methods:
- Utilized streptozotocin-induced diabetic rat models.
- Examined apoptosis, mitochondrial membrane potential (deltapsi), and protein levels (Bcl-2, Bax, Bcl-XL, cytochrome C) in DRG neurons.
- Assessed peripheral nerve conduction velocities (NCV).
Main Results:
- Diabetic rats exhibited increased apoptosis and altered mitochondrial membrane potential in DRG neurons.
- Mitochondrial dysfunction was evidenced by delayed recovery of deltapsi and cytochrome C translocation.
- Restoration of euglycemia normalized NCV, deltapsi, and apoptosis.
Conclusions:
- Apoptosis and mitochondrial dysfunction are key contributors to the pathogenesis of diabetic sensory neuropathy.
- Maintaining euglycemia may be crucial for preventing or reversing nerve damage in diabetic neuropathy.