The Effects of C-peptide on Type 1 Diabetic Polyneuropathies and Encephalopathy in the BBWor-rat

Abstract EN

Diabetic polyneuropathy (DPN) occurs more frequently in type 1 diabetes resulting in a more severe DPN.

The differences in DPN between the two types of diabetes are due to differences in the availability of insulin and C-peptide.

Insulin and C-peptide provide gene regulatory effects on neurotrophic factors with effects on axonal cytoskeletal proteins and nerve fiber integrity.

A significant abnormality in type 1 DPN is nodal degeneration.

In the type 1 BB/Wor-rat, C-peptide replacement corrects metabolic abnormalities ameliorating the acute nerve conduction defect.

It corrects abnormalities of neurotrophic factors and the expression of neuroskeletal proteins with improvements of axonal size and function.

C-peptide corrects the expression of nodal adhesive molecules with prevention and repair of the functionally significant nodal degeneration.

Cognitive dysfunction is a recognized complication of type 1 diabetes, and is associated with impaired neurotrophic support and apoptotic neuronal loss.

C-peptide prevents hippocampal apoptosis and cognitive deficits.

It is therefore clear that substitution of C-peptide in type 1 diabetes has a multitude of effects on DPN and cognitive dysfunction.

Here the effects of C-peptide replenishment will be extensively described as they pertain to DPN and diabetic encephalopathy, underpinning its beneficial effects on neurological complications in type 1 diabetes.