Glucose transporter expression on the plasma membrane of resting and activated white blood cells

Eur J Clin Invest. 2007 Apr;37(4):282-90. doi: 10.1111/j.1365-2362.2007.01786.x.


Background: In white blood cells (WBC), the increase in glucose utilization is a prominent feature during immune response and this depends on the function of specific glucose transporter (GLUT) isoforms. The objective was to examine the effects of activation by Phorbol 12-myristate 13-acetate (PMA) or lipopolysaccharide (LPS) and insulin on the expression of GLUT isoforms in all subpopulations of WBC.

Materials and methods: Blood was withdrawn from 27 healthy subjects. The expression of GLUT1, GLUT3 and GLUT4 on the plasma membrane of resting and activated monocytes, T- and B-lymphocytes and polymorphonuclear cells (PMNs) was determined in the absence and presence of physiological concentrations of insulin, by flow cytometry.

Results: GLUT1 did not respond to insulin in either resting or PMA/LPS activated state. In the resting state, monocytes and B-lymphocytes increased the abundance of GLUT3 and GLUT4 on their plasma membrane in response to insulin; in contrast, T-lymphocytes and PMNs were unresponsive to insulin. In the activated state, monocytes, B- and T- lymphocytes increased the expression of all three GLUT isoforms on their plasma membrane, whilst PMNs increased only GLUT1 and GLUT3; in all WBC, insulin augmented the expression of GLUT4 and GLUT3 isoforms in addition to the stimulation provided by the PMA or LPS treatment alone.

Conclusion: Activation of WBC leads to increased expression of GLUT1, GLUT3 and GLUT4 isoforms on their plasma membrane; this process was further augmented by insulin. During infection, these mechanisms may help to redistribute glucose as a potential source of energy away from peripheral tissues and direct it towards cells that mediate the immune response and are therefore crucial to survival.

MeSH terms

  • Adult
  • Androstadienes / pharmacology
  • Biological Transport / physiology
  • Cell Membrane / drug effects*
  • Cell Membrane / metabolism
  • Female
  • Glucose Transport Proteins, Facilitative / metabolism*
  • Humans
  • Hypoglycemic Agents / pharmacology
  • Insulin / metabolism
  • Insulin / pharmacology
  • Insulin Antagonists / pharmacology
  • Leukocytes / drug effects
  • Leukocytes / metabolism*
  • Lymphocyte Activation / physiology
  • Male
  • Wortmannin


  • Androstadienes
  • Glucose Transport Proteins, Facilitative
  • Hypoglycemic Agents
  • Insulin
  • Insulin Antagonists
  • Wortmannin