Table of Contents Author Guidelines Submit a Manuscript
Experimental Diabesity Research
Volume 4, Issue 4, Pages 235-256

The Insulin-Like Growth Factor System and Neurological Complications in Diabetes

1Department of Pathology, Wayne State University School of Medicine, Room 9275, H. G. Scott Hall, 540 East Canfield Avenue, Detroit, Michigan 48201, USA
2Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, USA
3Morris Hood Jr. Comprehensive Diabetes Center, Wayne State University School of Medicine, Detroit, Michigan, USA

Received 23 December 2002; Accepted 6 April 2003

Copyright © 2003 Hindawi Publishing Corporation. 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.


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.