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GLUT1-mediated glucose uptake plays a crucial role during Plasmodium hepatic infection

Patrícia Meireles1, Joana Sales-Dias1, Carolina M Andrade1

  • 1Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.

Cellular Microbiology
|July 13, 2016
PubMed

Insights

Glucose uptake is crucial for Plasmodium berghei malaria parasite development in the liver. Enhanced glucose transporter 1 (GLUT1) activity and membrane translocation support parasite growth, but inhibiting GLUT1 impairs infection.

Area of Science:

  • Parasitology
  • Cellular Biology
  • Infectious Diseases

Background:

  • Intracellular pathogens develop strategies for survival within host cells.
  • Hepatic infection by Plasmodium berghei, a rodent malaria parasite, is a complex process involving host-pathogen interactions.

Purpose of the Study:

  • To investigate the role of glucose metabolism and the glucose transporter 1 (GLUT1) in hepatic Plasmodium berghei infection.
  • To determine how host cells adapt to support parasite development.

Main Methods:

  • Studied glucose uptake in P. berghei-infected hepatic cells.
  • Assessed ATP levels and GLUT1 transporter activity and localization.
  • Utilized chemical inhibition of GLUT1 in vitro and in vivo.

Main Results:

  • P. berghei infection enhances glucose uptake via GLUT1 in infected cells.
  • Decreased cellular ATP levels correlate with increased GLUT1 activity.
  • GLUT1 translocates to the cell membrane, boosting glucose uptake during later infection stages.
  • Inhibition of GLUT1 activity reduces glucose uptake and impairs hepatic infection.

Conclusions:

  • Glucose and GLUT1 are critical for Plasmodium berghei hepatic development.
  • Host cells upregulate GLUT1 to maintain energy levels and support parasite growth.
  • Targeting GLUT1 presents a potential strategy for treating malaria.

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