الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Type 2 diabetes mellitus is growing around the world [1],[2]. It is intensively linked to obesity and insulin resistance [3],[4], and defects in the function and weight of the pancreatic β-cells [5],[6]. The vital regulatory effect of insulin on glucose, lipid, and protein metabolism is undermined by these metabolic disorders and thus causes a disorder in certain physiological processes. However, the development of honest diabetes takes years. Patients who develop T2DM have also been obese, along with an activated compensatory mechanism for ß cells such as excess basal insulin secretion and hyperproinsulinemia, As part of their metabolic profile [7]. These disease conditions occur early in the T2DM disease progression [8]. In a late stage (insulin-dependence) T2DM, βcell failures are serious. [8]. To combat T2DM, medications and therapeutic regimes are urgently needed. T2DM animal models are carefully described and clinically applicable to accomplish this goal of testing improved and experimental treatments. Both genetic models of spontaneous diabetes and non-spontaneous diabetes type experimentally induced occur. An example of a diabetes animal model that is experimentally induced is the rat treated HFD/STZ model. The present model combines a high-fat diet with sugar in some cases, which results in a significant reduction in the functional β-cell mass, hyperinsulinemia, Insulin resistance, and glucose-intolerance followed by treatment with β-cell toxin STZ (STZ). But in a shorter timeframe than in the human state, these two stressors are premeditated for the pathology of T2DM. [9]. Although on a shorter period of time than the human condition these two stressors are used together to mimic T2DM pathology.