Background: Type 2 diabetes mellitus (T2DM) is a chronic global disease characterized by serious complications. Evidence has shown that free radicals' formation is involved in the pathogenesis of the disease and development of its complications. T2DM is associated with disrupted glucose and lipid homeostasis with abnormal insulin sensitivity and/or secretion. No single treatment regimen is absolutely 100% effective. Metformin is a first-line treatment for T2DM whose main actions are the suppression of gluconeogenesis and the improvement of glucose uptake and insulin sensitivity. However, the exact mechanism of action is not clearly understood. Therefore, the current study aimed to assess the protective effects of metformin against diabetic complications in rats with explanation of the possible underlying mechanisms. Methods: rats were allocated in 3 groups. group1: control (C) received normal pellet diet (NPD), group2: diabetic (D) received high fat diet (HFD) for 2 weeks then injected intra-peritoneally (IP) with single low dose of streptozotocin (STZ) (30 mg/kg), group3: diabetic metformin treated (DM) received metformin 500 mg/kg/day by gavage for 4 weeks. Rats were sacrificed after 4 weeks of treatment. Results: The damaging effect of STZ on the pancreatic beta cells resulted in T2DM that was evaluated by assessment of glucose, insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), TGs, LDL, HDL, Urea, and malodialdehyde (MDA) in the diabetic rats 'serum. Conclusion: The results suggested the protective effects of metformin on ameliorating the diabetic effects