Sodium/glucose cotransporters display sodium and phlorizin
-dependent water permeability.
Loike, John D., Suzanne Hickman, Kunyan Kuang, Long Cao, Juan C. Vera,
Samuel C. Silverstein, and Jorge Fischbarg.
Rover Laboratory, Department of Physiology and Cellular Biophysics,
and the Department of Ophthalmology, Columbia Univ., New York, NY
10032; and (+) the Program in Molecular Pharmacology, Sloan Kettering
Memorial Cancer Center, New York, N.Y. 10021
APStracts 3:0210C, 1996.
Expression of Na+/glucose cotransporters of the SGLT1 type by Xenopus
laevis oocytes increased the osmotic permeability (Pf) of the oocytes
by a factor of 1.9-2.8, in the presence and in the absence of 5 mM
extracellular glucose. The Pf increase was correlated with the amount
of SGLT1 cRNA injected. In oocytes expressing SGLT1, either addition
of phlorizin to the medium or the replacement of Na+ by choline
inhibited the uptake of [alpha] -methyl-D-glucopyranoside, a specific
substrate for SGLT1, and returned oocyte Pf to its level in
uninjected oocytes. Phlorizin inhibited the SGLT1-attributable
increase in Pf with a Ki of 6.1 [mu]M, a value analogous to the Ki
for phlorizin inhibition of sugar uptake. However, neither the
presence of phlorizin nor the absence of extracellular Na+
significantly affected the increase in Pf elicited in oocytes
expressing GLUT1, a facilitative glucose transporter. These findings
suggest that SGLT1 forms a pore that allows the transmembrane passage
of water, and that water and glucose traverse the protein through
this pore. The finding that removal of extracellular Na+ abolishes
the increase in Pf attributable to SGLT1 suggests that extracellular
Na+ is required to maintain patency of this transporter's water
permeable transmembrane pore.
Received 26 February 1996; accepted in final form 18 June 1996.
APS Manuscript Number C101-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96