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New insights into the metabolic and molecular basis for diabetic neuropathy.
Cell Mol Life Sci 2003; 60(11):2445-64CM

Abstract

Diabetic polyneuropathy is the most common complication of diabetes mellitus. Several interactive pathogenetic mechanisms have been identified mainly in streptozotocin-induced diabetes in rats and have been ascribed to hyperglycemia. Over the last number of years it is becoming increasingly clear that diabetic neuropathy differs in type 1 and type 2 diabetes in humans and in murine models that more accurately mimic the human disorders. Beside hyperglycemia, attention is increasingly being paid to the pathogenetic roles of insulin and C-peptide deficiencies, particularly in type 1 diabetic neuropathy. There is now evidence to suggest that insulin and C-peptide deficiencies are mainly responsible for perturbations of neurotrophic factors and contribute to oxidative stress in diabetic nerve. This may also be true for apoptotic phenomena afflicting both the peripheral and central nervous systems in diabetes. The new data have lead to re-evaluations of pathogenetic components in this complex disorder, and their further exploration is likely to form a more refined basis for future therapeutic and preventive measures.

Authors+Show Affiliations

Departments of Pathology and Neurology and The Morris Hood Comprehensive Diabetes Center, Wayne State University, Scott Hall Rm 9275, 540 E Canfield Ave, Detroit, Michigan 48201, USA. asima@med.wayne.edu

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

14625688

Citation

Sima, A A F.. "New Insights Into the Metabolic and Molecular Basis for Diabetic Neuropathy." Cellular and Molecular Life Sciences : CMLS, vol. 60, no. 11, 2003, pp. 2445-64.
Sima AA. New insights into the metabolic and molecular basis for diabetic neuropathy. Cell Mol Life Sci. 2003;60(11):2445-64.
Sima, A. A. (2003). New insights into the metabolic and molecular basis for diabetic neuropathy. Cellular and Molecular Life Sciences : CMLS, 60(11), pp. 2445-64.
Sima AA. New Insights Into the Metabolic and Molecular Basis for Diabetic Neuropathy. Cell Mol Life Sci. 2003;60(11):2445-64. PubMed PMID: 14625688.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - New insights into the metabolic and molecular basis for diabetic neuropathy. A1 - Sima,A A F, PY - 2003/11/20/pubmed PY - 2004/1/6/medline PY - 2003/11/20/entrez SP - 2445 EP - 64 JF - Cellular and molecular life sciences : CMLS JO - Cell. Mol. Life Sci. VL - 60 IS - 11 N2 - Diabetic polyneuropathy is the most common complication of diabetes mellitus. Several interactive pathogenetic mechanisms have been identified mainly in streptozotocin-induced diabetes in rats and have been ascribed to hyperglycemia. Over the last number of years it is becoming increasingly clear that diabetic neuropathy differs in type 1 and type 2 diabetes in humans and in murine models that more accurately mimic the human disorders. Beside hyperglycemia, attention is increasingly being paid to the pathogenetic roles of insulin and C-peptide deficiencies, particularly in type 1 diabetic neuropathy. There is now evidence to suggest that insulin and C-peptide deficiencies are mainly responsible for perturbations of neurotrophic factors and contribute to oxidative stress in diabetic nerve. This may also be true for apoptotic phenomena afflicting both the peripheral and central nervous systems in diabetes. The new data have lead to re-evaluations of pathogenetic components in this complex disorder, and their further exploration is likely to form a more refined basis for future therapeutic and preventive measures. SN - 1420-682X UR - https://www.unboundmedicine.com/medline/citation/14625688/New_insights_into_the_metabolic_and_molecular_basis_for_diabetic_neuropathy_ L2 - https://dx.doi.org/10.1007/s00018-003-3084-x DB - PRIME DP - Unbound Medicine ER -