Although
insulin is known to affect neointimal
hyperplasia via distinct signaling pathways, how neointimal
hyperplasia is affected in insulin‑deficient type 1 diabetes remains unknown. The aim of the current study was to investigate two major signaling branches of
insulin action regulating neointimal
hyperplasia following arterial injury in
type 1 diabetes with or without exogenous
insulin administration. Rats were treated with vehicle (control group), streptozotocin (STZ) alone (STZ group; uncontrolled type 1 diabetes) or STZ followed by
insulin (STZ + I group; controlled type 1 diabetes). Subsequently, a type 1 diabetic rat model of carotid artery balloon injury was established. Following this, the intima‑to‑media area ratios were examined for evidence of neointimal
hyperplasia in the carotid arteries of the rats by performing hematoxylin‑eosin staining. Furthermore, the
protein expression of extracellular signal‑regulated
kinase (ERK), phosphorylated (p‑) ERK,
protein kinase B (Akt) and p‑Akt in the carotid arteries of the rats was determined via immunoblotting. Moreover, an in vitro model of type 1 diabetes was induced by incubation of primary vascular smooth muscle cells (VSMCs) with
glucose and/or
insulin. Cellular proliferation and signaling
protein expression levels in VSMCs were determined by measuring the incorporation of tritiated
thymidine and performing immunoblotting, respectively. The results demonstrated that compared with that in control rats, neointimal
hyperplasia and expression of p‑Akt in uncontrolled type 1 diabetic rats were significantly decreased. This decrease was recovered in controlled type 1 diabetes with
insulin therapy. Furthermore, the difference in the expression of p‑ERK between groups was not significant. Additionally, the results of the cell experiments were consistent with those from the animal studies. In conclusion, the preferential signaling along the phosphatidylinositol 3‑kinase/Akt pathway of
insulin action in response to
insulin restoration may contribute to neointimal
hyperplasia. The present study provides a novel approach for the further treatment of neointimal
hyperplasia in type 1 diabetes.