Effect of Carvacrol on PI3K/Akt Signaling, GLUT2 and Insulin Expression in Pancreatic Tissue in a Streptozotocin-Induced Type 1 Diabetic Rat Model

Background/Objectives: Diabetes mellitus is a major global health problem with increasing prevalence worldwide. Although the antidiabetic effects of carvacrol (CRV) have been reported, the molecular mechanisms underlying its action in pancreatic tissue remain unclear. The present study investigated the role of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in relation to glucose transporter 2 (GLUT2) and insulin expression in pancreatic tissue in a streptozotocin-induced type 1 diabetes mellitus rat model. Methods: Forty male Wistar albino rats were randomly divided into 5 groups: Sham, CRV, Streptozotocin (STZ), STZ + CRV 40, and STZ + CRV 20. At the beginning of the experiment, 55 mg/kg STZ was administered intraperitoneally to the diabetic groups. CRV was administered at the indicated doses for six weeks. Blood glucose levels were monitored weekly. The expression levels of PI3K, phosphorylated Akt (pAkt), and GLUT2 in pancreatic tissue were evaluated using immunohistochemical and Western blot analyses, whereas insulin expression was assessed by immunohistochemistry only. Results: Carvacrol treatment at 20 mg/kg was associated with significantly lower blood glucose levels compared with the STZ group from day 10 onward, whereas no significant difference was observed between the STZ + CRV 40 and STZ groups during the post-induction measurement period. Immunohistochemical and Western blot analyses demonstrated that PI3K, pAkt, and GLUT2 protein expression levels, which were decreased in the diabetic group, were significantly increased following 20 mg/kg carvacrol administration. Immunohistochemical analysis also showed increased insulin expression in this group. Conclusions: These findings suggest that carvacrol treatment may exert beneficial effects on glycemic control, accompanied by changes in PI3K/Akt phosphorylation-related signals and increased GLUT2 and insulin immunoreactivity in pancreatic tissue.