ABSTRACT:
This a model from the article:
Biophysical characteristics of the pig kidney Na+/glucose cotransporter SGLT2
reveal a common mechanism for SGLT1 and SGLT2.
Mackenzie B, Loo DD, Panayotova-Heiermann M, Wright EM. J Biol Chem
1996 Dec 20;271(51):32678-83 8955098
,
Abstract:
The Na+-dependent, low affinity glucose transporter SGLT2 cloned from pig kidney
is 76% identical (at the amino acid level) to its high affinity homologue SGLT1.
Using two-microelectrode voltage clamp, we have characterized the
presteady-state and steady-state kinetics of SGLT2 expressed in Xenopus oocytes.
The kinetic properties of the steady-state sugar-evoked currents as a function
of external Na+ and alpha-methyl-D-glucopyranoside (alphaMG) concentrations were
consistent with an ordered, simultaneous transport model in which Na+ binds
first. Na+ binding was voltage-dependent and saturated with hyperpolarizing
voltages. Phlorizin was a potent inhibitor of the sugar-evoked currents (KiPz
approximately 10 microM) and blocked an inward Na+ current in the absence of
sugar. SGLT2 exhibited Na+-dependent presteady-state currents with time
constants 3-7 ms. Charge movements were described by Boltzmann relations with
apparent valence approximately 1 and maximal charge transfer approximately 11
nC, and were reduced by the addition of sugar or phlorizin. The differences
between SGLT1 and SGLT2 were that (i) the apparent affinity constant (K0.5) for
alphaMG (approximately 3 mM) was an order of magnitude higher for SGLT2; (ii)
SGLT2 excluded galactose, suggesting discrete sugar binding; (iii) K0.5 for Na+
was lower in SGLT2; and (iv) the Hill coefficient for Na+ was 1 for SGLT2 but 2
for SGLT1. Simulations of the six-state kinetic model previously proposed for
SGLT1 indicated that many of the kinetic properties observed in SGLT2 are
expected by simply reducing the Na+/glucose coupling from 2 to 1.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Mackenzie B, Loo DD, Panayotova-Heiermann M, Wright EM. () - version=1.0
The original CellML model was created by:
Jonna Terkildsen
j.terkildsen@auckland.ac.nz
The University of Auckland
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
Camille Laibe 
