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"Parasite glucose metabolism" refers broadly to the suite of metabolic processes by which parasites such as *Plasmodium*, *Trypanosoma*, *Leishmania*, and *Cryptosporidium* extract and utilize glucose from their environment and host. Many pathogenic protozoa rely heavily (sometimes exclusively) on glycolysis for ATP production, especially in their infectious blood stages, due to reduced or absent mitochondrial metabolism[2][3][4][6][7][9][10]. Parasites possess hexose transporters and glycolytic enzymes, some of which differ biochemically from host homologs. Inhibition of these transporters or enzymes can selectively kill parasites with lesser effects on host cells, making components of glucose metabolism attractive but challenging drug targets. This pathway is implicated in infection pathogenicity, with metabolic adaptations affecting disease severity and parasite survival. Targeting parasite glucose metabolism is an established strategy in antiparasitic drug development, but it is not itself a discrete molecule or drug target in the classical sense[2][3][5][6][9][10].
Inhibition of glucose uptake (hexose transporters/GLUT family orthologs) Inhibition of key glycolytic enzymes (hexokinase, aldolase, glyceraldehyde-3-phosphate dehydrogenase, lactate dehydrogenase, etc.) Disruption of ATP production and energy metabolism
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