title: Enhanced expression of glucose transporter 1 on erythrocyte membrane in hemodialysis patients: the possible role in erythrocyte ascorbate recycling.
abstract: BACKGROUND
  Human erythrocytes can take up dehydroascorbate on the glucose transporter 1 (GLUT 1) and reduce it to ascorbate. Intraerythrocyte ascorbate was proved to be directly responsible for decreased oxidation of extraerythrocytic ascorbate. In addition to spontaneous and irreversible loss of ascorbate in plasma, the hemodialysis (HD) process itself consumes plasma ascorbate. However, intraerythrocyte ascorbate status in uremic patients during HD has yet to be reported.
  
  
  METHODS
  Plasma and intraerythrocyte ascorbate, dehydroascorbate, GLUT 1 expression on erythrocyte membranes, and in vitro studies of "erythrocyte ascorbate recycling" were investigated in age- and sex-matched healthy subjects (control group) and HD patients (HD group).
  
  
  RESULTS
  Intraerythrocyte ascorbate concentrations decreased after 1 HD session compared with pre-HD and recovered to pre-HD values 2 days later, whereas plasma ascorbate concentrations did not recover. In vitro studies suggested that erythrocytes of HD patients have a stronger ability to maintain intracellular ascorbate concentrations compared with healthy subjects. This ability could be inhibited by cytochalasin B (GLUT 1 inhibitor). We also found increased GLUT 1 expression (P = 0.002) on erythrocyte membranes in the HD group compared with the control group.
  
  
  CONCLUSIONS
  Erythrocytes of uremic patients lost large amounts of ascorbate during HD, but regained it to the pre-HD level 2 days later. Enhanced GLUT 1 expression on erythrocyte membranes for HD patients may contribute to better preservation of intracellular ascorbate compared with healthy subjects.
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Joseph G
authors.initials: JG
authors.lastname: Wann
authors.forename: Chien-Sheng
authors.initials: CS
authors.lastname: Lin
authors.forename: Li-Chien
authors.initials: LC
authors.lastname: Chang
authors.forename: Yung-Ho
authors.initials: YH
authors.lastname: Hsu
authors.forename: Chiang-Ting
authors.initials: CT
authors.lastname: Chien
authors.forename: Deborah W
authors.initials: DW
authors.lastname: Tai
authors.forename: Jin-Shuen
authors.initials: JS
authors.lastname: Chen
authors.forename: Chih-Ching
authors.initials: CC
authors.lastname: Yang
authors.forename: Lai-King
authors.initials: LK
authors.lastname: Yeung
authors.forename: Chau-Fong
authors.initials: CF
authors.lastname: Chen
mesh_terms: D000368:Aged; D001205:Ascorbic Acid / Q000097:blood* / Q000502:physiology*; D015153:Blotting, Western; D002851:Chromatography, High Pressure Liquid; D003571:Cytochalasin B / Q000494:pharmacology; D003683:Dehydroascorbic Acid / Q000097:blood; D004910:Erythrocyte Membrane / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D004912:Erythrocytes / Q000737:chemistry / Q000187:drug effects / Q000502:physiology; D005260:Female; D051272:Glucose Transporter Type 1 / Q000032:analysis / Q000037:antagonists & inhibitors / Q000097:blood* / Q000502:physiology; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D013997:Time Factors; D014511:Uremia / Q000097:blood / Q000503:physiopathology / Q000628:therapy
chemical_list: D051272:Glucose Transporter Type 1; D003571:Cytochalasin B; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid