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One of the most prevalent metabolic diseases, type 2 diabetes mellitus (T2DM), is brought on by a combination of two main factors: the pancreatic β-cells' impaired ability to secrete insulin and the tissues' inability to react to insulin as needed [1]. Type 2 diabetes mellitus (T2DM) is one of the most common chronic metabolic diseases, featuring hyperglycemia resulting from resistance to insulin action and an inadequate compensatory insulin secretory response. The lasting chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and complications, such as diabetic nephropathy, cardiovascular disease (CVD), and retinopathy. These complications threaten the lifespan and the quality of life in T2DM patients [2, 3–4].
The recent epidemic of diabetes mellitus, along with advancements in the treatment of diabetes and its complications, has led to a rapid increase in the number of aged patients with diabetes [5, 6–7]. The global prevalence of T2DM quadrupled between 1980 and 2014 and already grossly exceeds the predictions made in 2000 for the year 2030 by both the International Diabetes Federation and the World Health Organization [8, 9]. Three primary biological abnormalities that underlie this disease are insulin resistance, beta cell apoptosis, and insufficient insulin production. This metabolic condition occurs by an increase in blood sugar levels in the body due to a decrease in insulin, an increase in the creation of glucose, or a decrease in the intake of glucose. Regular monitoring of blood glucose levels and regular visits to medical facilities are necessary [10]. Some of the most important symptoms of diabetes include high blood sugar, frequent urination (polyuria), hunger (polyphagia), excessive thirst (polydipsia), weight loss despite a large appetite, and blurred vision [11]. Researchers that have examined the complex relationship between genetic predisposition and diabetes in great detail have identified a number of genetic variants to type 2 diabetes [12]. Various genes are linked to diabetes. For example, the Fat mass and obesity-associated (FTO) gene is associated with obesity, but the insulin receptor substrate gene (IRS1) and the peroxisome proliferator-activated receptor gene (PPARG) reduce insulin sensitivity. The LPL gene can influence the development of type 2 diabetes by metabolizing lipids, while glucokinase regulatory gene (GCKR) affects it by stimulating GCK activity and lowering blood...