Prospective Role of ÃÂ²-Cell-Specific IGF-1 for Oxidative Stress in the Pathogenesis of Diabetic NeuropathySeigo Usuki*
Institute of Molecular Medicine and Genetics, Georgia Health Sciences University, Augusta, USA
- *Corresponding Author:
- Seigo Usuki
PhD, Seigo Usuki
Frontier Research Center for Post-genome Science and Technology
Hokkaido University, Sapporo, Hokkaido
E-mail: [email protected]
Received date: May 02, 2012; Accepted date: May 25, 2012; Published date: May 28, 2012
Citation: Usuki S (2012) Prospective Role of ß-Cell-Specific IGF-1 for Oxidative Stress in the Pathogenesis of Diabetic Neuropathy. J Diabetes Metab S5:009. doi:10.4172/2155-6156.S5-009
Copyright: © 2012 Usuki S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Diabetic neuropathy is a well-known complication of diabetes mellitus. The mechanism for progression of diabetic neuropathy is unclear, but many risk factors, such as abnormalities of glucose metabolism and oxidative stress, have been given much attention for their contributory role in the loss or degeneration of neurons. Homocysteine is a risk factor of cardiovascular disease and diabetes/metabolic disease. Homocysteine metabolism is dependent on vitamin B12 the deficiency of which induces peripheral neuropathy. On the other hand, the examination of generative pathology showed the potential involvement of many growth factors in neuroprotection and regeneration. This review implicates Insulin-like growth factor-1(IGF-1) as playing a crucial role in pancreatic β-cell functions and homocysteine-induced oxidative stress. A defense mechanism against diabetic neuropathy via homocysteine-induced oxidative stress due to a protective effect of β-cell-specific IGF-1 will be discussed.