Thyroid hormone action on glucose transporter activity in astrocytes.
In astrocytes from rat brain cultured in thyroid hormone-deficient media cytochalasin B-binding was decreased 80%; addition of L-T3 increased binding to 75% of control levels. Saponin-treatment of controls increased accessibility of binding sites to 60% above untreated cells. Saponin also increased binding in deficient cells; however, the level was less than in treated controls, suggesting L-T3 deficiency decreases total glucose transporters. Addition of L-T3 appeared to convert most (90%) of the binding sites from unavailable to accessible status. Changes in binding to plasma membranes in response to L-T3 level were similar to those in intact cells. No binding to Golgi was detectable, thus no evidence for translocation of carriers was obtained. L-T3 may activate the glucose transporter by increasing its accessibility in brain cells.
Roeder
L M
LM
Department of Pediatrics, University of Maryland, School of Medicine, Baltimore.
Hopkins
I B
IB
Kaiser
J R
JR
Hanukoglu
L
L
Tildon
J T
JT
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D003470:Culture Media; D003571:Cytochalasin B / Q000378:metabolism; D006056:Golgi Apparatus / Q000187:drug effects / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D014284:Triiodothyronine / Q000494:pharmacology*
D003470:Culture Media; D009004:Monosaccharide Transport Proteins; D014284:Triiodothyronine; D003571:Cytochalasin B