Glucose Consumption of Plasmodium hexamerium

Glucose Transport in the Malarial (Plasmodium lophurae) Infected Erythrocyte*

“…Observations on the consumption of glucose by "erythrocyte-free" P. lophurue (FP) showed that these cells were considerably more active than malaria-infected red cells. Therefore, it was concluded that glucose utilization by P. lophurae-infected erythrocytes was in harmony with the results obtained for other species of malaria (1,8,9,11,18). Glucose entry.-The entry of glucose into both the normal and malaria-infected red cell followed Michaelis-Menten kinetics at low concentrations (Below 2 mM).…”

“…Indeed, one of the most striking characteristics of the malaria-infected erythrocyte is its high rate of glucose consumption. For example, in the monkey malaria, Plasmodium knowlesi, the parasitized erythrocyte consumes up to 25 times more glucose than a normal cell ( 1 I ) , and in the bird malarias, P. gallinaceum, P. hexamerium, and P. relictum, glucose utilization by infected red cells is 5 to 10 fold greater than uninfected cells (8,9,18).…”

An overview of the Plasmodium falciparum hexose transporter and its therapeutic interventions

“…They proposed that two components, a simple diffusion system on the erythrocyte plasma membrane (EPM) and a proton-coupled active glucose transporter on the PPM, might be involved in the glucose uptake in parasitized erythrocytes. 36,37 Subsequent research from Kirk et al confirmed the accumulation of 14 C-2-DOG in P. falciparum-infected human erythrocytes and discovered that the phosphorylation of 2-DOG, rather than active transport, accounted for the substrate accumulation. 36,38 Given that the intracellular/extracellular ratios of 3-OMG and L-glucose were kept below 1, Kirk et al concluded that the glucose uptake of parasitized erythrocytes works through an equilibrium manner rather than via active transport.…”

“…Morphological and physical changes of malaria-infected erythrocytes have long been recognized, which result in the perturbation of erythrocytic substrate permeability of sodium, potassium, and amino acids. [28][29][30][31] The concept that glucose permeability of parasitized erythrocytes might also be altered can be dated back to 1966 when Herman and colleagues investigated the 14 C-D-glucose utilization of P. gallinaceum-infected chicken erythrocytes. 32,33 They found that the parasitized chicken erythrocytes produced more 14 CO 2 derived from 14 C-D-glucose and speculated that the uptake of glucose was increased by parasite infection.…”

“…[28][29][30][31] The concept that glucose permeability of parasitized erythrocytes might also be altered can be dated back to 1966 when Herman and colleagues investigated the 14 C-D-glucose utilization of P. gallinaceum-infected chicken erythrocytes. 32,33 They found that the parasitized chicken erythrocytes produced more 14 CO 2 derived from 14 C-D-glucose and speculated that the uptake of glucose was increased by parasite infection. 32 The first experimental evidence of accelerated glucose uptake in parasitized erythrocytes was reported in 1974.…”