Abstract
We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-βII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.
Original language | English (US) |
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Pages (from-to) | 2609-2614 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 582 |
Issue number | 17 |
DOIs | |
State | Published - Jul 23 2008 |
Externally published | Yes |
Keywords
- Cell adhesion molecule
- Diabetes mellitus
- Inflammation
- Nitric oxide
- Signal transduction
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology