Thyroid hormone increases the partitioning of glucose transporters
to the plasma membrane in arl 15 cells: cell surface glut1
photolabeling with atb-[3h]bmpa.
Haber, Richard S., Cindy M. Wilson, Steven P. Weinstein, Alla
Pritsker, and Samuel W. Cushman.
Department of Medicine, The Mount Sinai School of Medicine, One
Gustave L. Levy Place, New York, NY 10029, Experimental Diabetes,
Metabolism, and Nutrition Section, Diabetes Branch, National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health, Bethesda, MD 20892
APStracts 2:0088E, 1995.
The stimulation of glucose transport by T3 in the liver-derived ARL 15
cell line is only partly attributable to increased GLUT1 glucose
transporter gene expression. To test the hypothesis that T3 increases
the partitioning of GLUT1 to the cell surface, we quantitated surface
GLUT1 using the photolabel ATB-[3H]BMPA. In control cells only about
20% of total cellular GLUT1 was present at the cell surface. T3
treatment (100 nM) for 6 h increased the rate of [3H]2-deoxyglucose
(2-DG) uptake by 30%, 92%, and 95% in three experiments, and
increased surface GLUT1 photolabeling by 17%, 81%, and 72%,
respectively, with no increase in total cellular GLUT1. T3 treatment
for 48 h increased [3H]2-DG uptake by 143%, 172%, and 216% in three
experiments and increased cell surface GLUT1 photolabeling by 88%,
161%, and 184%, respectively, with smaller increases in total
cellular GLUT1. T3 treatment for 48 h thus increased the fraction of
cellular GLUT1 at the plasma membrane, from 21 +/- 2% to 35 +/- 3%
(means +/- SE). We conclude that most of the early (6 h) stimulation
of glucose transport by T3 in ARL 15 cells is mediated by an increase
in the partitioning of GLUT1 to the plasma membrane. With more
chronic T3 treatment (48 h), the enhanced surface partitioning of
GLUT1 is persistent, and is superimposed on an increase in total
cellular GLUT1, accounting for a further increase in glucose
transport.
Received 5 December 1994; accepted in final form 18 April 1995.
APS Manuscript Number E505-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.