<p>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.</p> <p>Substantial evidence collected from clinical data and experimental
studies has indicated that CNS is not spared
from diabetes complications. Impairments in CNS function
are well documented in both type 1 and type 2 diabetic
patients as well as in various animal models of diabetes,
in terms of alterations in cognition, neuropsychology, neurobehavior,
electrophysiology, structure, neurochemistry
and apoptotic activities. These data suggest that <italic>primary
diabetic encephalopathy</italic> exists as a definable diabetic complication.
The mechanisms underlying this CNS complication
are not clear. Experimental studies have suggested that
neuronal apoptosis may play an important role in neuronal
loss and impaired cognitive function. In diabetes multiple
factors are responsible for neuronal apoptosis, such as a perturbed
IGF system, hyperglycemia and the aging process
itself. Recent data suggest that insulin/C-peptide deficiency
may exert an eminent role. Administration of C-peptide
partially corrects the perturbed IGF system in the brain
and prevents neuronal apoptosis in hippocampus of type 1
diabetes. In neuroblastoma SH-SY5Y cells C-peptide provides
a dose-dependent stimulation on cell proliferation and
an anti-apoptotic effect as well. These studies provide a basis
for administration of C-peptide as a potentially effective
therapy for type 1 diabetes.</p>
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Exp Diabesity Res. 2004; 5(1):79-90