The therapeutic effects of arginine on hyperglycemia, pancreatic α/β cells, oxidative stress, and bone turnover markers (CTx and OPG) in alloxan-induced diabetic rats.

This study evaluated the therapeutic effects of arginine (Arg) on hyperglycemia, pancreatic α/β cells integrity, oxidative stress biomarkers, C-telopeptide (CTx), and osteoprotegerin (OPG) in a rat model of alloxan-induced diabetes mellitus. A total of 36 male Wistar rats, weighing 126.14 ± 3.25 g and aged 75.47 ± 2.25 days (means ± SD), were randomly allocated into three equal group: control group (CG), diabetic control group (DCG), and arginine-supplemented diabetic group (Arg-DCG). Arg was administered orally at 400 mg/kg body weight daily for 28 days following diabetic confirmed. The DCG developed sustained hyperglycemia throughout the study period compared to the CG and Arg-DCG. Regarding oxidative stress, the Arg-DCG showed significant improvements in the antioxidant enzymes glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) compared to the DCG. Conversely, malondialdehyde (MDA) a marker of lipid peroxidation, was significantly higher in the DCG relative to the CG, with only partial attenuation observed in the Arg-DCG. Western blot analysis showed a significant increase in relative CTx band intensity and a significant decrease in relative OPG band intensity in the Arg-DCG compared to DCG. Furthermore, qPCR analysis revealed that OPG gene expression (2^-ΔΔ Ct) was significantly higher in the Arg-DCG compared to the CG (2.03 vs 1.00), but remained lower than that of the DCG (2.03 vs 2.46). Histopathological analysis revealed significant improvements in pancreatic α/β cell repair in the Arg-DCG compared to the DCG, showcasing better-defined islets, reduced degeneration, and intact acinar tissue, suggesting partial protection from alloxan-induced damage. In conclusion, arginine therapy may effectively alleviate hyperglycemia, preserve pancreatic α/β cell integrity, and enhance antioxidant defense mechanisms in alloxan-induced diabetic rats.