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Glucose utilization refers to the collective biological processes through which cells uptake and metabolize glucose to produce adenosine triphosphate (ATP) and biosynthetic precursors [1, 16]. This process is a fundamental aspect of cellular energy homeostasis and is primarily regulated by the hormone insulin, which promotes glucose entry into peripheral tissues like skeletal muscle and adipose tissue by triggering the translocation of the GLUT4 transporter to the cell membrane [3, 8, 19]. In metabolic disorders such as Type 2 diabetes mellitus, glucose utilization is significantly impaired due to insulin resistance or deficiency, leading to chronic hyperglycemia and systemic complications [15, 16, 18]. Conversely, malignant cells often exhibit accelerated glucose utilization through aerobic glycolysis, known as the Warburg effect, to sustain rapid proliferation and survival in the tumor microenvironment [2, 7, 9]. Pharmacological interventions aim to modulate this process by enhancing insulin sensitivity, stimulating glucose uptake, or inhibiting hepatic gluconeogenesis to restore glycemic control [1, 3, 15]. Monitoring of glucose utilization in clinical and research settings is commonly performed using biomarkers such as HbA1c or imaging techniques like FDG-PET [1, 7, 16].
Drugs modulate glucose utilization by stimulating the translocation of glucose transporters (e.g., GLUT4), activating AMP-activated protein kinase (AMPK) to increase glycolytic flux, inhibiting hepatic gluconeogenesis, or enhancing insulin receptor signaling sensitivity.
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