C-peptide and Central Nervous System Complications in Diabetes

摘要

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 primary diabetic encephalopathy 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-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.