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Unmyelinated fiber sensory neuropathy differs in type 1 and type 2 diabetes.
Diabetes Metab Res Rev. 2005 Sep-Oct; 21(5):448-58.DM

Abstract

BACKGROUND

Neuropathic pain is common in diabetic patients. Degeneration of sensory C-fibers in peripheral nerve plays a prominent role in the generation of neuropathic pain. We examined degenerative changes of C-fibers in two rat models with type 1 and type 2 diabetes.

METHODS

Type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor-rats of 8 months duration with equal exposure to hyperglycemia were examined. Thermal hyperalgesia was monitored using an infrared thermal probe. C-fiber size, number, frequencies of denervated Schwann cells, regenerating C-fibers, type 2 axon/Schwann cell relationship and collagen pockets in the sural nerve were examined morphometrically. Neurotrophic receptor expression was examined by Western blotting. Neurotrophins and neuropeptides were examined by ELISA.

RESULTS

Type 1 rats showed increased thermal hyperalgesia followed by a decrease. Hyperalgesia in type 2 rats showed a slower progression. These findings were associated with a 50% (p < 0.001) loss of C-fibers, increased frequencies of denervated Schwann cells (p < 0.001), regenerating fibers (p < 0.001), collagen pockets (p < 0.001) and type 2 axon/Schwann cell relationship (p < 0.001) in type 1, but not in type 2 rats. Expression of insulin receptor, IGF-1R, TrkA and C was decreased in BB/Wor rats, whereas BBZDR/Wor rats showed milder or no deficits. NGF and NT-3 in sciatic nerve and substance P and calcitonin gene-related peptide in dorsal root ganglia were decreased in type 1, but not in type 2 rats.

CONCLUSION

The more severe molecular, functional and morphometric abnormalities of nociceptive C-fibers in type 1 insulinopenic rats compared to type 2 hyperinsulinemic rats suggest that impaired insulin action may play a more important pathogenetic role than hyperglycemia per se.

Authors+Show Affiliations

Department of Pathology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15747389

Citation

Kamiya, Hideki, et al. "Unmyelinated Fiber Sensory Neuropathy Differs in Type 1 and Type 2 Diabetes." Diabetes/metabolism Research and Reviews, vol. 21, no. 5, 2005, pp. 448-58.
Kamiya H, Murakawa Y, Zhang W, et al. Unmyelinated fiber sensory neuropathy differs in type 1 and type 2 diabetes. Diabetes Metab Res Rev. 2005;21(5):448-58.
Kamiya, H., Murakawa, Y., Zhang, W., & Sima, A. A. (2005). Unmyelinated fiber sensory neuropathy differs in type 1 and type 2 diabetes. Diabetes/metabolism Research and Reviews, 21(5), 448-58.
Kamiya H, et al. Unmyelinated Fiber Sensory Neuropathy Differs in Type 1 and Type 2 Diabetes. Diabetes Metab Res Rev. 2005;21(5):448-58. PubMed PMID: 15747389.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Unmyelinated fiber sensory neuropathy differs in type 1 and type 2 diabetes. AU - Kamiya,Hideki, AU - Murakawa,Yuichi, AU - Zhang,Weixian, AU - Sima,Anders A F, PY - 2005/3/5/pubmed PY - 2005/10/22/medline PY - 2005/3/5/entrez SP - 448 EP - 58 JF - Diabetes/metabolism research and reviews JO - Diabetes Metab. Res. Rev. VL - 21 IS - 5 N2 - BACKGROUND: Neuropathic pain is common in diabetic patients. Degeneration of sensory C-fibers in peripheral nerve plays a prominent role in the generation of neuropathic pain. We examined degenerative changes of C-fibers in two rat models with type 1 and type 2 diabetes. METHODS: Type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor-rats of 8 months duration with equal exposure to hyperglycemia were examined. Thermal hyperalgesia was monitored using an infrared thermal probe. C-fiber size, number, frequencies of denervated Schwann cells, regenerating C-fibers, type 2 axon/Schwann cell relationship and collagen pockets in the sural nerve were examined morphometrically. Neurotrophic receptor expression was examined by Western blotting. Neurotrophins and neuropeptides were examined by ELISA. RESULTS: Type 1 rats showed increased thermal hyperalgesia followed by a decrease. Hyperalgesia in type 2 rats showed a slower progression. These findings were associated with a 50% (p < 0.001) loss of C-fibers, increased frequencies of denervated Schwann cells (p < 0.001), regenerating fibers (p < 0.001), collagen pockets (p < 0.001) and type 2 axon/Schwann cell relationship (p < 0.001) in type 1, but not in type 2 rats. Expression of insulin receptor, IGF-1R, TrkA and C was decreased in BB/Wor rats, whereas BBZDR/Wor rats showed milder or no deficits. NGF and NT-3 in sciatic nerve and substance P and calcitonin gene-related peptide in dorsal root ganglia were decreased in type 1, but not in type 2 rats. CONCLUSION: The more severe molecular, functional and morphometric abnormalities of nociceptive C-fibers in type 1 insulinopenic rats compared to type 2 hyperinsulinemic rats suggest that impaired insulin action may play a more important pathogenetic role than hyperglycemia per se. SN - 1520-7552 UR - https://www.unboundmedicine.com/medline/citation/15747389/Unmyelinated_fiber_sensory_neuropathy_differs_in_type_1_and_type_2_diabetes_ L2 - https://doi.org/10.1002/dmrr.541 DB - PRIME DP - Unbound Medicine ER -