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Cellular and physiological effects of C-peptide
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Hills, Claire E. and Brunskill, Nigel J. (2009) Cellular and physiological effects of C-peptide. Clinical Science, Vol.116 (No.7). pp. 565-574. doi:10.1042/CS20080441 ISSN 0143-5221.
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Official URL: http://dx.doi.org/10.1042/CS20080441
Abstract
In recent years, accumulating evidence indicates a biological function for proinsulin C-peptide. These results challenge the traditional view that C-peptide is essentially inert and only useful as a surrogate marker of insulin release. Accordingly, it is now clear that C-peptide binds with high affinity to cell membranes, probably to a pertussis-toxin-sensitive G-protein-coupled receptor. Subsequently, multiple signalling pathways are potently and dose-dependently activated in multiple cell types by C-peptide with the resulting activation of gene transcription and altered cell phenotype. In diabetic animals and Type I diabetic patients, short-term studies indicate that C-peptide also enhances glucose disposal and metabolic control. Furthermore, results derived from animal models and clinical studies in Type I diabetic patients suggest a salutary effect of C-peptide in the prevention and amelioration of diabetic nephropathy and neuropathy. Therefore a picture of Type I diabetes as a dual-hormone-deficiency disease is developing, suggesting that the replacement of C-peptide alongside insulin should be considered in its management.
Item Type: | Journal Article | ||||
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Subjects: | Q Science > Q Science (General) | ||||
Divisions: | Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- ) | ||||
Journal or Publication Title: | Clinical Science | ||||
Publisher: | Portland Press | ||||
ISSN: | 0143-5221 | ||||
Official Date: | 2009 | ||||
Dates: |
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Volume: | Vol.116 | ||||
Number: | No.7 | ||||
Number of Pages: | 10 | ||||
Page Range: | pp. 565-574 | ||||
DOI: | 10.1042/CS20080441 | ||||
Status: | Peer Reviewed | ||||
Publication Status: | Published | ||||
Access rights to Published version: | Restricted or Subscription Access |
Data sourced from Thomson Reuters' Web of Knowledge
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