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International Journal of Experimental Diabetes Research
Volume 3, Issue 4, Pages 241-245

C-Peptide Prevents Hippocampal Apoptosis in Type 1 Diabetes

1Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan, USA
2Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan MI 48201, USA
3Morris J. Hood Jr. Comprehensive Diabetes Center, Wayne State University School of Medicine, Detroit, Michigan, USA
4Department of Pathology, Wayne State University School of Medicine, Room 9275, H.G. Scott Hall, 540 East Canfield Avenue 48201, Detroit, Michigan, USA

Received 4 June 2002; Accepted 1 August 2002

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To explore mechanisms underlying central nervous system (CNS) complications in diabetes, we examined hippocampal neuronal apoptosis and loss, and the effect of C-peptide replacement in type 1 diabetic BB/W rats. Apoptosis was demonstrated after 8 months of diabetes, by DNA fragmentation, increased number of apoptotic cells, and an elevated ratio of Bax/Bcl-xL, accompanied by reduced neuronal density in the hippocampus. No apoptotic activity was detected and neuronal density was unchanged in 2-month diabetic hippocampus, whereas insulin-like growth factor (IGF) activities were impaired. In type 1 diabetic BB/W rats replaced with C-peptide, no TdT-mediated dUTP nick-end labeling (TUNEL)- positive cells were shown and DNA laddering was not evident in hippocampus at either 2 or 8 months. C-peptide administration prevented the preceding perturbation of IGF expression and reduced the elevated ratio of Bax/Bcl-xL. Our data suggest that type 1 diabetes causes a duration-dependent programmed cell death of the hippocampus, which is partially prevented by C-peptide.