title: IGF-I increases the recruitment of GLUT4 and GLUT3 glucose transporters on cell surface in hyperthyroidism.
abstract: OBJECTIVE
  In hyperthyroidism, tissue glucose disposal is increased to adapt to high energy demand. Our aim was to examine the regulation of glucose transporter (GLUT) isoforms by IGF-I in monocytes from patients with hyperthyroidism.
  
  
  METHODS
  Blood (20 ml) was drawn from 21 healthy and 10 hyperthyroid subjects. The abundance of GLUT isoforms on the monocyte plasma membrane was determined in the absence and presence of IGF-I (0.07, 0.14, and 0.7 nM) using flow cytometry. Anti-CD14-phycoerythrin monocional antibody was used for monocyte gating. GLUT isoforms were determined after staining the cells with specific antisera to GLUT3 and GLUT4.
  
  
  RESULTS
  In monocytes from the euthyroid subjects, IGF-I increased the abundance of GLUT3 and GLUT4 on the monocyte surface by 25 and 21% respectively (P<0.0005 with repeated measures ANOVA). Hyperthyroidism increased the basal monocyte surface GLUT3 and GLUT4; in these cells, IGF-I had a marginal but highly significant effect (P=0.003, with repeated measures ANOVA) on GLUT3 (11%) and GLUT4 (10%) translocation on the plasma membrane.
  
  
  CONCLUSIONS
  In hyperthyroidism: 1) basal abundance of GLUT3 and GLUT4 on the plasma membrane is increased and 2) the sensitivity of the recruitment of GLUT3 and GLUT4 transporters on the plasma membrane in response to IGF-I is increased. These findings may contribute to the understanding of the mechanism by which hyperthyroidism increases glucose disposal in peripheral tissues.
authors.affiliation: Second Department of Internal Medicine, Research Institute and Diabetes Center, University General Hospital Attikon, Athens University, 1 Rimini Street, 12462 Haidari, Greece. gdimi@ath.forthnet.gr
authors.forename: George
authors.initials: G
authors.lastname: Dimitriadis
authors.forename: Eirini
authors.initials: E
authors.lastname: Maratou
authors.forename: Eleni
authors.initials: E
authors.lastname: Boutati
authors.forename: Anastasios
authors.initials: A
authors.lastname: Kollias
authors.forename: Katerina
authors.initials: K
authors.lastname: Tsegka
authors.forename: Maria
authors.initials: M
authors.lastname: Alevizaki
authors.forename: Melpomeni
authors.initials: M
authors.lastname: Peppa
authors.forename: Sotirios A
authors.initials: SA
authors.lastname: Raptis
authors.forename: Dimitrios J
authors.initials: DJ
authors.lastname: Hadjidakis
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D005434:Flow Cytometry; D051274:Glucose Transporter Type 3 / Q000378:metabolism*; D051275:Glucose Transporter Type 4 / Q000378:metabolism*; D006801:Humans; D006980:Hyperthyroidism / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D009000:Monocytes / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D051274:Glucose Transporter Type 3; D051275:Glucose Transporter Type 4; D007328:Insulin; C495687:SLC2A3 protein, human; C495692:SLC2A4 protein, human; D007334:Insulin-Like Growth Factor I