Abstract
The IGF system plays vital roles in neuronal development,
metabolism, regeneration and survival. It consists of
IGF-I, IGF-II, insulin, IGF-I-receptor, and those of IGF-II
and insulin as well as IGF-binding proteins. In the last
decades it has become clear that perturbations of the IGF
system play important roles in the pathogenesis of diabetic
neurological complications. In the peripheral nervous system
IGF-I, insulin, and C-peptide particularly in type 1 diabetes
participate in the development of axonal degenerative
changes and contributes to impaired regenerative capacities.
These abnormalities of the IGF system appear to be
less pronounced in type 2 diabetes, which may in part account
for the relatively milder neurological complications
in this type of diabetes. The members of the IGF system
also provide anti-apoptotic effects on both peripheral and
central nervous system neurons. Furthermore, both insulin
and C-peptide and probably IGF-I possess gene regulatory
capacities on myelin constituents and axonal cytoskeletal
proteins. Therefore, replenishment of various members of
the IGF system provides a reasonable rational for prevention
and treatment of diabetic neurological complications.