## 1 Introduction  
Diabetes mellitus (DM) is a chronic disorder associated with a group of metabolic derangements characterized by elevated blood sugar levels, frequent urination, increased hunger and increased appetite. DM can lead to several untreated problems, such as diabetic ketoacidosis, hyperosmalor hyperglyic disorders or death [1]. Severe, long-lasting risks include heart failure, chronic kidney disease, foot ulcers, nerve damage, eye injury and cognitive disability [2; 3]. DM has three major types. Type 1 diabetes is attributed to the pancreas' inability to produce adequate insulin associated with beta-cell loss [4]. Type 2 diabetes begins with insulin resistance, where cells respond incorrectly to insulin. Gestational diabetes is the third primary type that occurs when pregnant women experience elevated blood sugar levels without a prior history of DM [5]. Oxidative stress (OS) is caused by an imbalance between oxygen-derived radicals and the organism's antioxidant potential. This disrupts the natural cellular balance between radical production and defense. This causes oxidative damage to proteins, lipids and nucleic acids [6]. OS leads to an enormous number of diseases over time, including DM, atherosclerosis, inflammatory conditions, hypertension, heart disease, neurodegenerative diseases and cancer [7; 8]. Oxidative stress is enhanced in both insulin-dependent and non-insulin-dependent diabetes. In addition, increasing the generation of free radicals and oxidative stress is a critical event in the development of the micro-and macrovascular complications of diabetes [3]. This hypothesis has been supported by the demonstration of elevated levels of oxidative stress biomarkers in patients with type 2 diabetes who are suffering from complications of their disease [9]. As a result, it appears plausible to assume that antioxidants can play a significant role in the improvement of diabetic symptoms. Various studies have linked diabetes to increased free radical formation and decreased antioxidant capacity [9]. Furthermore, numerous studies have been conducted on the impact of antioxidants in the management of diabetes [9]. Dyslipidemia is an abnormal level of lipids in the blood (e.g., triglycerides, fat phospholipids and cholesterol). Dyslipidemia is one of the most significant risk factors for DM and cardiovascular disease [10]. Atherosclerosis is accelerated in both type 1 and type 2 and is induced in diabetic patients by dyslipidemia [11]. Dyslipidemia in diabetic patients suggests the presence of what is known as the lipid triad: hypertriglyceridemia, low levels of high-density lipoprotein (HDL) and high levels of low-density lipoprotein (LDL) [10; 12]. However, other studies have reported normal or minimally elevated total cholesterol levels in diabetic patients despite the risk of cardiovascular disease [13]. Hyperglycemia due to DM stimulates glucose self-oxidation to produce free radicals, which contribute to macro and microvascular dysfunction [14]. DM can lower antioxidant protection by reducing plasma/serum status or free radical scavenging activity, and increasing plasma-oxidization levels of specific antioxidant agents like ascorbic acid and vitamin E. Furthermore, people with type 2 diabetes showed a decrease in the endothelial synthesis of nitric oxide (NO) [15]. Current clinical trials consider the therapeutic potential of medications for DM based on the present understanding of the pathogenesis of diabetic complications. However, studies on antidiabetic drug efficacy have raised significant concerns, such as the effects of the medications on antioxidant properties [16], serum lipid profiles [17], blood glucose levels and overall safety [18]. Renal disease is a severe and recurrent DM complication. Kidney damage in DM may occur due to arterial (renovascular) and microvascular (classic diabetic renal disease) factors [19]. Furthermore, DM is the major reason for end-stage renal disease (ESRD). Controlling the glucose level is the best method to avoid diabetic kidney diseases [20].