الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Diabetes mellitus (DM), a prevalent chronic disease, arises from either a complete lack or reduced effectiveness of insulin (Eizirik et al., 2020). Among different types, type 2 DM (T2DM) dominates clinical encounters (Zhu et al., 2018). This form of diabetes is marked by insulin resistance, where tissues become less responsive to insulin’s effects (Sandeep & Nandini, 2017). A key feature of this resistance lies in disrupted signaling within the insulin/PI3K/Akt pathway, ultimately leading to increased activity of a protein called glycogen synthase kinase-3 beta (GSK-3β) (Zhang et al., 2018). Another crucial player in cellular energy sensing and metabolic balance, AMP-activated protein kinase (AMPK), also plays a role. Dysfunction in AMPK activity has been allied to the development of both insulin resistance and T2DM (Coughlan et al., 2014).T2DM is a multifaceted condition marked by a gradual decline in the effectiveness of insulin, together with the failure of β-cells to adequately counteract insulin resistance (Mohamed et al., 2020). A recent study has verified that the combination of a diet rich in fat with a low dosage of streptozotocin (STZ) treatment is an excellent alternative animal model for evaluating antidiabetic substances (Abdou et al., 2022). In the high-fat diet (HFD)/STZ diabetic model, HFD consumption leads to insulin resistance, while a small amount of STZ therapy initially impairs the activity of β-cells, closely resembling the natural metabolic processes observed in human T2DM.