## 1 Introduction  
Type 2 diabetes mellitus (T2 DM) is distinguished by its unique characteristics, encompassing disruptions in carbohydrate, lipid, and protein metabolism. This complex condition arises from compromised insulin secretion and resistance. T2 DM holds particular significance due to its substantial prevalence, accounting for over 90% of all diabetes cases, in contrast to the less common type 1 diabetes mellitus (T1 DM) [1]. T2 DM is a chronic and intricate disorder that requires ongoing medical attention, self-management for the regulation of glucose levels, and blood pressure control to prevent both microvascular complications (including retinopathy, neuropathy, and nephropathy) and macrovascular complications (such as heart attacks and strokes) [2; 3; 4]. As of now, a definitive cure for T2 DM remains elusive. However, available treatment approaches encompass lifestylemodifications, interventions for managing obesity, the administration of oral hypoglycemic agents, and insulin sensitizers, with metformin being the recommended first-line medication for obese patients [5]. Oral hypoglycemic agents are categorized based on their distinct mechanisms of action, which include inhibition of \(\alpha\)-glucosidase and \(\alpha\)-amylase in the digestive tract, influence on glucose uptake and transporter activity, enhancement of insulin secretion, promotion of pancreatic \(\beta\) cell proliferation, antioxidative properties to mitigate oxidative stress, and inhibitory activity of protein tyrosine phosphatase [6]. The insulin receptor necessitates the tyrosine autophosphorylation of three closely situated tyrosine residues within its kinase domain to facilitate subsequent insulin-induced glucose uptake. Recent efforts have been directed towards enhancing overall insulin action by mitigating the inhibitory effects on initial insulin responses. This is achieved by modulating the activity of cellular protein tyrosine phosphatases (PTPs), which serve as potential targets for therapeutic intervention [7]. Among these PTPs are PTP1B, PTPN2, PTPN11, PTPN9, PTPRS, and DUSP9, which collectively contribute to the induction of insulin resistance, making them attractive targets for treating T2 DM [8]. PTP1B and PTPN9 function as negative regulators of insulin signaling pathways by dephosphorylating the insulin receptor. The absence of PTPN2 enhances insulin receptor activation in both hepatocytes and fibroblasts. PTPN11 serves as a negative regulator in the liver, and its deletion enhances hepatic insulin sensitivity [8; 9]. Mice lacking PTPRS exhibit alterations in insulin sensitivity and glucose homeostasis [10]. DUSP9, located on the X chromosome, encodes a member of the mitogen-activated protein kinase phosphatase 4 family, playing a pivotal role in cell cycle regulation and the regulation of insulin action [11]. _Ginkgo biloba_ (Ginkgoaceae) has played significant roles as a valuable plant for humans. Its history spans over 200 years, earning it the distinction of being a \"living fossil\". _G. biloba_ was introduced to Europe around 1730 and has since become a prominent tree in streets and parks. It has also found extensive use as a medicinal plant, particularly in China and Korea [12]. The leaves of _G. biloba_ are traditionally employed in the treatment of diarrhea and infantile enteritis, while its seeds have been used to address various conditions such as ringworm sores, pox, dog bites, asthma, phlegm, and colds [13]. _G. biloba_ contains a variety of beneficial compounds, including terpene trilatoclones (bilobalide), flavonoids (kaemperfol, quercetin, and their glycosides), bioflavonoids (ginkgetin), proanthocyanidis (procyanidin), and alkylphenols (ginkgolic acids) [14]. Recent studies have indicated that extracts from _G. biloba_ leaves exhibit a wide range of beneficial properties, including antiashmatic, antioxidant, wound healing, radical-scavenging, neuroprotective, and metabolic syndrome management effects, which include weight loss, antidiabetic, and antihypertensive properties [12; 15].