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Glucose transport and metabolic pathways represent the integrated biological systems responsible for the movement of glucose across cell membranes and its subsequent biochemical conversion into energy or storage forms. This broad category includes the facilitative glucose transporter (GLUT) family and the sodium-glucose linked transporter (SGLT) family, which mediate glucose entry into cells and renal reabsorption, respectively (Navale & Paranjape, 2016). Once inside the cell, glucose enters metabolic sequences such as glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle to generate ATP and biosynthetic precursors (Nelson & Cox, 2017). Dysregulation of these processes is central to the pathogenesis of Type 2 diabetes mellitus, metabolic syndrome, and various cancers, where metabolic reprogramming (the Warburg effect) supports rapid cell proliferation (Petersen & Shulman, 2018). Therapeutic strategies often focus on specific nodes within these pathways, such as inhibiting SGLT2 to lower blood sugar or activating AMPK to improve metabolic efficiency (Rena et al., 2017). Given the essential nature of glucose for brain and systemic function, pharmacological modulation must be carefully managed to prevent adverse effects like severe hypoglycemia (Wright, 2021).
Drugs targeting these pathways act through various mechanisms including the inhibition of renal glucose reabsorption via SGLT2 inhibitors, suppression of hepatic gluconeogenesis by biguanides, stimulation of pancreatic insulin secretion by sulfonylureas, and enhancement of peripheral insulin sensitivity through thiazolidinediones (Rena et al., 2017; Wright, 2021).
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