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Type 1 diabetic neuropathy and C-peptide.
Exp Diabesity Res 2004 Jan-Mar; 5(1):65-77ED

Abstract

The most common microvascular diabetic complication, diabetic peripheral polyneuropathy (DPN), affects type 1 diabetic patients more often and more severely. In recent decades, it has become increasingly clear that perpetuating pathogenetic mechanisms, molecular, functional, and structural changes and ultimately the clinical expression of DPN differ between the two major types of diabetes. Impaired insulin/C-peptide action has emerged as a crucial factor to account for the disproportionate burden affecting type 1 patients. C-peptide was long believed to be biologically inactive. However, it has now been shown to have a number of insulin-like glucose-independent effects. Preclinical studies have demonstrated dose-dependent effects on Na+,K(+)-ATPase activity, endothelial nitric oxide synthase (eNOS), and endoneurial blood flow. Furthermore, it has regulatory effects on neurotrophic factors and molecules pivotal to the integrity of the nodal and paranodal apparatus and modulatory effects on apoptotic phenomena affecting the diabetic nervous system. In animal studies, C-peptide improves nerve conduction abnormalities, prevents nodal degenerative changes, characteristic of type 1 DPN, promotes nerve fiber regeneration, and prevents apoptosis of central and peripheral nerve cell constituents. Limited clinical trials have confirmed the beneficial effects of C-peptide on autonomic and somatic nerve function in patients with type 1 DPN. Therefore, evidence accumulates that replacement of C-peptide in type 1 diabetes prevents and even improves DPN. Large-scale food and drug administration (FDA)-approved clinical trials are necessary to make this natural substance available to the globally increasing type 1 diabetic population.

Authors+Show Affiliations

Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA. asima@med.wayne.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

15198372

Citation

Sima, Anders A F., et al. "Type 1 Diabetic Neuropathy and C-peptide." Experimental Diabesity Research, vol. 5, no. 1, 2004, pp. 65-77.
Sima AA, Zhang W, Grunberger G. Type 1 diabetic neuropathy and C-peptide. Exp Diabesity Res. 2004;5(1):65-77.
Sima, A. A., Zhang, W., & Grunberger, G. (2004). Type 1 diabetic neuropathy and C-peptide. Experimental Diabesity Research, 5(1), pp. 65-77.
Sima AA, Zhang W, Grunberger G. Type 1 Diabetic Neuropathy and C-peptide. Exp Diabesity Res. 2004;5(1):65-77. PubMed PMID: 15198372.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Type 1 diabetic neuropathy and C-peptide. AU - Sima,Anders A F, AU - Zhang,Weixian, AU - Grunberger,George, PY - 2004/6/17/pubmed PY - 2004/10/13/medline PY - 2004/6/17/entrez SP - 65 EP - 77 JF - Experimental diabesity research JO - Exp. Diabesity Res. VL - 5 IS - 1 N2 - The most common microvascular diabetic complication, diabetic peripheral polyneuropathy (DPN), affects type 1 diabetic patients more often and more severely. In recent decades, it has become increasingly clear that perpetuating pathogenetic mechanisms, molecular, functional, and structural changes and ultimately the clinical expression of DPN differ between the two major types of diabetes. Impaired insulin/C-peptide action has emerged as a crucial factor to account for the disproportionate burden affecting type 1 patients. C-peptide was long believed to be biologically inactive. However, it has now been shown to have a number of insulin-like glucose-independent effects. Preclinical studies have demonstrated dose-dependent effects on Na+,K(+)-ATPase activity, endothelial nitric oxide synthase (eNOS), and endoneurial blood flow. Furthermore, it has regulatory effects on neurotrophic factors and molecules pivotal to the integrity of the nodal and paranodal apparatus and modulatory effects on apoptotic phenomena affecting the diabetic nervous system. In animal studies, C-peptide improves nerve conduction abnormalities, prevents nodal degenerative changes, characteristic of type 1 DPN, promotes nerve fiber regeneration, and prevents apoptosis of central and peripheral nerve cell constituents. Limited clinical trials have confirmed the beneficial effects of C-peptide on autonomic and somatic nerve function in patients with type 1 DPN. Therefore, evidence accumulates that replacement of C-peptide in type 1 diabetes prevents and even improves DPN. Large-scale food and drug administration (FDA)-approved clinical trials are necessary to make this natural substance available to the globally increasing type 1 diabetic population. SN - 1543-8600 UR - https://www.unboundmedicine.com/medline/citation/15198372/Type_1_diabetic_neuropathy_and_C_peptide_ L2 - https://dx.doi.org/10.1080/15438600490424541 DB - PRIME DP - Unbound Medicine ER -