期刊
DIABETOLOGIA
卷 51, 期 1, 页码 175-182出版社
SPRINGER
DOI: 10.1007/s00125-007-0853-3
关键词
diabetes; C-peptide; glucose transport; GLUT1; chromium; erythrocytes
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL073942] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK071888] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL 073942] Funding Source: Medline
- NIDDK NIH HHS [R01 DK071888-02, R01 DK071888, DK 071888] Funding Source: Medline
Aims/hypothesis Proinsulin C-peptide has been implicated in reducing complications associated with diabetes and also in improving blood flow. We hypothesised that incubation of erythrocytes with C-peptide would improve the ability of these cells to release ATP, a stimulus for nitric oxide production. Methods Erythrocytes obtained from rabbits (n=11) and both healthy and type 2 diabetic humans (n=7) were incubated with C-peptide in the absence and presence of Fe2+ and Cr-3+,Cr- and the resulting ATP release was measured via chemiluminescence. This release was also measured in the presence and absence of phloretin, an inhibitor of GLUT1, and also of mannose, a glycolysis inhibitor. To determine glucose transport, C-14-labelled glucose was added to erythrocytes in the presence and absence of the C-peptide-metal complex and the aforementioned inhibitors. Results The release of ATP from the erythrocytes of patients with diabetes increased from 64 +/- 13 to 260 +/- 39 nmol/l upon incubation of the cells in C-peptide. The C-peptide activity was dependent upon binding to Fe2+ which was extended upon binding to Cr3+. The increase in ATP release from the erythrocytes is due to metal-activated C-peptide stimulation of glucose transfer into the erythrocytes via the GLUT1 transporter. In the presence of C-peptide complexed to Cr3+ the amount of glucose transferred into the erythrocyte increased by 31%. Conclusions/interpretation When complexed to Fe2+ or Cr3+ C-peptide has the ability to promote ATP release from erythrocytes. This release is due to an increase in glucose transport through GLUT1.
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