SYNOPSIS Plasmodium lophurae‐infected red blood cells utilized considerably greater quantities of glucose than did uninfected duckling red cells. Kinetic analysis of glucose transport showed: (A). Below a concentration of 2 mM in the medium the uptake process followed Michaelis‐Menten kinetics (carrier‐mediated facilitated diffusion) whereas at concentrations greater than this simple diffusion became the main mode of entry. (B). The apparent transport constants, Kt, for normal and infected cells were similar. However there was an 8‐fold increase in the maximal velocity, Vmax, for infected cells. (C). “Free” malaria parasites had a significantly lower Kt and a higher Vmax than did normal or infected red cells. Entry and exit studies with the nonmetabolizable sugar analog, 3‐0‐methyl glucose, demonstrated that the enhanced rate of uptake by infected cells involved an increase in the simple diffusion component and the degree of enhancement was correlated with the size of the intracellular parasite. Competition experiments suggested that in the malaria‐infected cell one locus is involved in the carrier‐mediated transport of glucose, mannose and galactose whereas another locus transports fructose and/or glycerol. These results indicate that the enhanced entry of glucose into the malaria‐infected red cell is a consequence of factors other than increased glucose catabolism by the host‐parasite complex, and the host cell's capacity to take up greater quantities of sugar directly involves the growing intracellular plasmodium.

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