Intracellular Signalling by C-Peptide

Joint Authors

Hills, Claire E.
Brunskill, Nigel J.

Source

Experimental Diabetes Research

Issue

Vol. 2008, Issue 2008 (31 Dec. 2008), pp.1-8, 8 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2008-03-18

Country of Publication

Egypt

No. of Pages

8

Main Subjects

Diseases

Abstract EN

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+/K+ 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.

American Psychological Association (APA)

Hills, Claire E.& Brunskill, Nigel J.. 2008. Intracellular Signalling by C-Peptide. Experimental Diabetes Research،Vol. 2008, no. 2008, pp.1-8.
https://search.emarefa.net/detail/BIM-486929

Modern Language Association (MLA)

Hills, Claire E.& Brunskill, Nigel J.. Intracellular Signalling by C-Peptide. Experimental Diabetes Research No. 2008 (2008), pp.1-8.
https://search.emarefa.net/detail/BIM-486929

American Medical Association (AMA)

Hills, Claire E.& Brunskill, Nigel J.. Intracellular Signalling by C-Peptide. Experimental Diabetes Research. 2008. Vol. 2008, no. 2008, pp.1-8.
https://search.emarefa.net/detail/BIM-486929

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-486929