Conclusion

It is clear from these data that the neuropathies occurring in the two BB-rat models show distinct differences in underlying metabolic and molecular changes, progression of functional deficits and the spectra of morphological changes despite the same exposure to hyperglycemia. Therefore the differences imply that hyperglycemia is only one component of the pathogenetic web underlying DPN. The other major component contributing to DPN is provided by the deficiencies in insulin and synergistically acting C-peptide, resulting in impaired insulin signaling. These latter defects appear to substantially add to the severity of the neural Na+/K+-ATPase defect and to be the major culprit in the perturbations of impaired neurotrophic support, and to be the sole factor in the development of nodal/paranodal dysfunction and pathology. Hence, these differences in underlying mechanisms explain the differences in the progression and severity between type 1 and type 2 DPN. Only by recognizing such differences in underlying factors and their associated dynamic consequences in the development of DPN will it be possible to approach these disorders therapeutically in biologically meaningful ways, as already documented by several successful C-peptide trials in type 1 DPN.

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