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|Title:||Intracellular signalling by C-peptide.|
|Authors:||Hills, Claire E.|
Brunskill, Nigel J.
|Publisher:||Hindawi Publishing Corporation|
|Citation:||Experimental Diabetes Research, Volume 2008 (2008), Article ID 635158|
|Abstract:||C-peptide, a cleavage product of the proinsulin molecule, has long been regarded as biologically inert, serving merely as a surrogate marker for insulin release. Recent findings demonstrate both a physiological and protective role of C-peptide when administered to individuals with type I diabetes. Data indicate that C-peptide appears to bind in nanomolar concentrations to a cell surface receptor which is most likely to be G-protein coupled. Binding of C-peptide initiates multiple cellular effects, evoking a rise in intracellular calcium, increased PI-3-kinase activity, stimulation of the Na[superscript +]/K[superscript +] ATPase, increased eNOS transcription, and activation of the MAPK signalling pathway. These cell signalling effects have been studied in multiple cell types from multiple tissues. Overall these observations raise the possibility that C-peptide may serve as a potential therapeutic agent for the treatment or prevention of long-term complications associated with diabetes.|
|Rights:||Copyright © 2008 C. E. Hills and N. J. Brunskill. 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.|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
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|10.1155_2008_635158.pdf||Published (publisher PDF)||2.05 MB||Adobe PDF||View/Open|
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