Effect of dietary L-arginine supplementation on the expression of vascular endothelial growth factor A, its receptors, and nitric oxide system components in the pancreas of streptozotocin-induced diabetic rats.

T1DM is characterized by elevated blood glucose levels, insulin insufficiency, and alterations in vessel formation. Therefore, the expression of insulin, active caspase-3, inflammatory factors such as TNF-α and NF-κB, and components of the NO and VEGFA systems were investigated in the pancreas of STZ-induced diabetic rats. Blood glucose levels and body weight were also measured. Additionally, the effects of L-arginine supplementation on the same parameters were evaluated. The body weight of the STZ and STZ + L-arginine groups was lower than that of the control and L-arginine groups. L-arginine supplementation reduced blood glucose levels and increased insulin levels in diabetic rats. Degenerative changes in β-cells were observed in the pancreas of the diabetic group. Insulin expression was low in the STZ-group, while it was higher in the STZ + L-arginine group. VEGFA was localized in the islets, epithelial cells of glands, tubules, and endothelial cells in both the control and L-arginine groups. A similar localization pattern was observed for VEGFA in the STZ and STZ + L-arginine groups. Expression of eNOS and VEGFR2/FLK1/KDR was detected in the islets of the control and L-arginine groups. Their expression was low in the STZ and STZ + L-arginine groups. However, VEGFR2/FLK1/KDR signal intensity was stronger in STZ + L-arginine group than in the STZ group. The expression levels of iNOS, active caspase-3, TNF-α, and NF-κB were significantly higher in STZ group than in the control group. In conclusion, although L-arginine treatment reversed STZ-induced hyperglycemia and insulin deficiency, it did not exert a significant effect on the expression levels of iNOS, active caspase-3, TNF-α, or NF-κB. Additionally, L-arginine appears essential for islet vessel maintenance by increasing VEGFR2/FLK1/KDR expression.