title: Quantity of Na/K-ATPase and glucose transporters in the plasma membrane of rat adipocytes is reduced by in vivo triiodothyronine.
abstract: The expression of sodium-potassium pumps and glucose transporters in pure adipocyte plasma membranes from a hyperthyroid animal model was studied. Hyperthyroidism was induced by enteral administration of five doses of 90 micrograms of triiodothyronine every second day to 8-week-old rats. Following isolation of epididymal adipocytes, 3-O-methylglucose transport was measured and the number of Na/K-ATPase-(alpha 1- and alpha 2-isoforms) and glucose transporter (GLUT1 and GLUT4) molecules in sheets of adipocyte plasma membrane were determined by quantitative immunoelectron microscopy, using gold labelling. Maximal in vitro insulin stimulation of adipocytes increased the glucose transport rate and the amount of GLUT4 in the plasma membrane 15-fold, whereas the amount of alpha 2 was unaffected. In adipocytes from hyperthyroid rats, mean adipocyte volume was decreased by 18% and the quantities of GLUT4 per unit area of plasma membrane (maximal insulin stimulation) and of alpha 2 were decreased by 19% and 15%, respectively. Thus, hypotrophia of fat tissue in the hyperthyroid state is associated with a decreased expression in the plasma membrane of the glucose transporter GLUT4 and the alpha 2-isoform of Na/K-ATPase.
authors.affiliation: Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
authors.forename: M
authors.initials: M
authors.lastname: Voldstedlund
authors.forename: J
authors.initials: J
authors.lastname: Tranum-Jensen
authors.forename: A
authors.initials: A
authors.lastname: Handberg
authors.forename: J
authors.initials: J
authors.lastname: Vinten
mesh_terms: D019325:3-O-Methylglucose; D017667:Adipocytes / Q000737:chemistry* / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D001692:Biological Transport / Q000502:physiology; D001786:Blood Glucose / Q000032:analysis; D002462:Cell Membrane / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D006980:Hyperthyroidism / Q000201:enzymology / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D007536:Isomerism; D008297:Male; D008757:Methylglucosides / Q000378:metabolism / Q000493:pharmacokinetics; D016253:Microscopy, Immunoelectron; D009004:Monosaccharide Transport Proteins / Q000032:analysis* / Q000378:metabolism; D009124:Muscle Proteins; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis* / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology*
chemical_list: D001786:Blood Glucose; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D007328:Insulin; D008757:Methylglucosides; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495679:Slc2a1 protein, rat; C495694:Slc2a4 protein, rat; D014284:Triiodothyronine; D019325:3-O-Methylglucose; D000254:Sodium-Potassium-Exchanging ATPase