Figure 6.

Proposed model of GLUT1‐mediated glucose uptake during hepatic infection by Plasmodium. Following the invasion of hepatic cells by Plasmodium parasites and the establishment of infection (left), parasites initiate a process of dramatic intracellular replication. Parasite development reduces the amount of host intracellular glucose, leading to depletion of the ATP pool and binding of ADP/AMP to GLUT1 transporters at the plasma membrane. This results in their activation (middle). At later stages of infection, GLUT1 transporters present in the host cell's cytoplasmic compartments are translocated to the cell membrane, leading to further enhancement of glucose uptake (right).