Effects of Carvacrol on PI3K/Akt Pathway, Glut2 and Insulin Expression in Pancreatic Cells in a Rat Model of Type 1 Diabetes Mellitus

Diabetes mellitus is an important disease whose prevalence is rapidly increasing every year due to genetic predisposition, malnutrition, inactivity, and obesity. The antidiabetic properties of Carvacrol (CRV) have been demonstrated in previous studies; however, it is not known through which pathway it exerts this effect in pancreatic tissue. Therefore, in our study, we planned to demonstrate the expression changes of the PI3K/Akt pathway, Glut2, and Insulin proteins in pancreatic tissue using immunohistochemical and Western-blot methods to investigate the mechanism by which CRV achieves this effect. For this purpose, 40 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 6 weeks. As a result of the experiment, a statistically significant decrease in blood glucose levels was detected in the STZ+CRV 20 and STZ+CRV 40 groups compared to the STZ group. It was found that a 20 mg/kg dose of CRV administered to the diabetic group was more effective in reducing blood glucose levels. It was shown by immunohistochemical and Western blot examination that PI3K, pAkt, Glut2, and Insulin protein expressions, which were decreased in the diabetic group, were significantly increased by 20 mg/kg Carvacrol administration. This study concluded that Carvacrol activates the PI3K/Akt pathway in pancreatic tissue in diabetes mellitus, increases Glut2 and insulin expression, and thus has a lowering effect on blood glucose levels.