C-peptide and Central Nervous System Complications in Diabetes |
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Authors: | Zhen-guo Li Anders A. F. Sima |
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Affiliation: | 1. Department of Pathology, Wayne State University School of Medicine, Room 9275, H.G. Scott Hall, 540 East Canfield Avenue, Detroit, Michigan, 48201, USA.;2. Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, USA.;3. Morris J. Hood Jr. Comprehensive Diabetes Center, Wayne State University School of Medicine, Detroit, Michigan, USA, |
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Abstract: | Substantial evidence collected from clinical data and experimentalstudies has indicated that CNS is not sparedfrom diabetes complications. Impairments in CNS functionare well documented in both type 1 and type 2 diabeticpatients as well as in various animal models of diabetes,in terms of alterations in cognition, neuropsychology, neurobehavior,electrophysiology, structure, neurochemistryand apoptotic activities. These data suggest that primarydiabetic encephalopathy exists as a definable diabetic complication.The mechanisms underlying this CNS complicationare not clear. Experimental studies have suggested thatneuronal apoptosis may play an important role in neuronalloss and impaired cognitive function. In diabetes multiplefactors are responsible for neuronal apoptosis, such as a perturbedIGF system, hyperglycemia and the aging processitself. Recent data suggest that insulin/C-peptide deficiencymay exert an eminent role. Administration of C-peptidepartially corrects the perturbed IGF system in the brainand prevents neuronal apoptosis in hippocampus of type 1diabetes. In neuroblastoma SH-SY5Y cells C-peptide providesa dose-dependent stimulation on cell proliferation andan anti-apoptotic effect as well. These studies provide a basisfor administration of C-peptide as a potentially effectivetherapy for type 1 diabetes. |
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