| Autor: |
Elbassuoni EA; a Physiology Department, Minia University Faculty of Medicine, Minia 61111, Egypt., Aziz NM; a Physiology Department, Minia University Faculty of Medicine, Minia 61111, Egypt., El-Tahawy NF; b Histology and Cell Biology Department, Minia University Faculty of Medicine, Minia 61111, Egypt. |
| Jazyk: |
angličtina |
| Zdroj: |
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme [Appl Physiol Nutr Metab] 2018 Jun; Vol. 43 (6), pp. 617-624. Date of Electronic Publication: 2018 Jan 19. |
| DOI: |
10.1139/apnm-2017-0617 |
| Abstrakt: |
Diabetic nephropathy one of the major microvascular diabetic complications. Besides hyperglycemia, other factors contribute to the development of diabetic complications as the proinsulin connecting peptide, C-peptide. We described the role of C-peptide replacement therapy on experimentally induced diabetic nephropathy, and its potential mechanisms of action by studying the role of nitric oxide (NO) as a mediator of C-peptide effects by in vivo modulating its production by N G -nitro-l-arginine methyl ester (L-NAME). Renal injury markers measured were serum urea, creatinine, tumor necrosis factor alpha, and angiotensin II, and malondialdehyde, total antioxidant, Bcl-2, and NO in renal tissue. In conclusion, diabetic induction resulted in islet degenerations and decreased insulin secretion with its metabolic consequences and subsequent renal complications. C-Peptide deficiencies in diabetes might have contributed to the metabolic and renal error, since C-peptide treatment to the diabetic rats completely corrected these errors. The beneficial effects of C-peptide are partially antagonized by L-NAME coadministration, indicating that NO partially mediates C-peptide effects. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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