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International Journal of Experimental Diabetes Research - Volume 3 2002, Issue 4, Pages 241-245



Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan, USA

Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan MI 48201, USA

Morris J. Hood Jr. Comprehensive Diabetes Center, Wayne State University School of Medicine, Detroit, Michigan, USA

Department 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.

Abstract

To explore mechanisms underlying central nervous systemCNS complications in diabetes, we examined hippocampal neuronalapoptosis and loss, and the effect of C-peptide replacementin type 1 diabetic BB-W rats. Apoptosis was demonstrated after8 months of diabetes, by DNA fragmentation, increased number ofapoptotic cells, and an elevated ratio of Bax-Bcl-xL, accompaniedby reduced neuronal density in the hippocampus. No apoptotic activitywas detected and neuronal density was unchanged in 2-monthdiabetic hippocampus, whereas insulin-like growth factor IGF activitieswere impaired. In type 1 diabetic BB-W rats replaced withC-peptide, no TdT-mediated dUTP nick-end labeling TUNEL-positive cells were shown and DNA laddering was not evident inhippocampus at either 2 or 8 months. C-peptide administration preventedthe preceding perturbation of IGF expression and reducedthe elevated ratio of Bax-Bcl-xL. Our data suggest that type 1 diabetescauses a duration-dependent programmed cell death of thehippocampus, which is partially prevented by C-peptide.





Autor: Zhen-guo Li, Weixian Zhang, and Anders A. F. Sima

Fuente: https://www.hindawi.com/



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