title: Glucose transporter expression on the plasma membrane of resting and activated white blood cells.
abstract: 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.
  
  
  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  Blood was withdrawn from 27 healthy subjects.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.
  
  
  CONCLUSIONS
  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.
authors: Hellenic National Diabetes Center, Athens, Greece.
authors: E
authors: E
authors: Maratou
authors: G
authors: G
authors: Dimitriadis
authors: A
authors: A
authors: Kollias
authors: E
authors: E
authors: Boutati
authors: V
authors: V
authors: Lambadiari
authors: P
authors: P
authors: Mitrou
authors: S A
authors: SA
authors: Raptis
mesh_terms: D000328:Adult; D000730:Androstadienes / Q000494:pharmacology; D001692:Biological Transport / Q000502:physiology; D002462:Cell Membrane / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D051246:Glucose Transport Proteins, Facilitative / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology; D007329:Insulin Antagonists / Q000494:pharmacology; D007962:Leukocytes / Q000187:drug effects / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000502:physiology; D008297:Male; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D051246:Glucose Transport Proteins, Facilitative; D007004:Hypoglycemic Agents; D007328:Insulin; D007329:Insulin Antagonists; D000077191:Wortmannin