C-Peptide is Relevant in Type 1 Diabetes and its Complications: Summary and Conclusions to the Special Issue

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Abstract
The Review of Diabetic Studies,2009,6,3,223-224.
Published:November 2009
Type:Review Article
Authors:
Author(s) affiliations:

John Wahren1 and Anders A.F. Sima2,3

1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.

2Department of Pathology, Wayne State University, Detroit, MI, USA. 3 Department of Neurology, Wayne State University, Detroit, MI, USA.

Abstract:

It has been very satisfying to put together this Special Edition of The Review of Diabetic Studies on C-peptide and diabetes. We are greatly encouraged by the advances being made in this research area, and especially to see the beneficial effects of C-peptide making their way into clinic. Once regarded as a redundant waste product of insulin synthesis, C-peptide is now recognized as an important regulatory hormone in its own right. Our understanding of C-peptide physiology is expanding rapidly. It is abundantly clear that C-peptide deficiency in type 1 diabetes plays important pathogenetic roles in the development of various complications, with consequent beneficial effects upon C-peptide replacement. Over the last decade and a half, a wealth of new information has accumulated regarding Cpeptide’s interaction with a variety of cell types, its intracellular signaling mechanisms, and its impact on specific cell functions, as well as growth and cell death. It also emerges from these reviews that several questions remain, e.g. the conundrum of C-peptide’s interaction with the cell membrane remains unresolved. Is there a C-peptide receptor which, to date, has escaped detection? It is clear that C-peptide binds to cell membranes and accumulates in endosomes in the cytoplasm. Also, it exerts effects on major signaling pathways such as the MAPK and PI-3 kinase pathways with fundamental influences on Na+/K+-ATPase and eNOS acivities. These activities affect renal, peripheral nerve, and vascular functions. Read more...

Keywords:Nil