This study examines the conformations of the Na(+)/glucose cotransporter (SGLT1) during sugar transport using charge and fluorescence measurements on the human SGLT1 mutant G507C expressed in Xenopus oocytes. The mutant exhibited similar steady-state and presteady-state kinetics as wild-type SGLT1, and labeling of Cys507 by tetramethylrhodamine-6-maleimide had no effect on kinetics. Our strategy was to record changes in charge and fluorescence in response to rapid jumps in membrane potential in the presence and absence of sugar or the competitive inhibitor phlorizin. In Na(+) buffer, step jumps in membrane voltage elicited presteady-state currents (charge movements) that decay to the steady state with time constants tau(med) (3-20 ms, medium) and tau(slow) (15-70 ms, slow). Concurrently, SGLT1 rhodamine fluorescence intensity increased with depolarizing and decreased with hyperpolarizing voltages (DeltaF). The charge vs. voltage (Q-V) and fluorescence vs. voltage (DeltaF-V) relations (for medium and slow components) obeyed Boltzmann relations with similar parameters: zdelta (apparent valence of voltage sensor) approximately 1; and V(0.5) (midpoint voltage) between -15 and -40 mV. Sugar induced an inward current (Na(+)/glucose cotransport), and reduced maximal charge (Q(max)) and fluorescence (DeltaF(max)) with half-maximal concentrations (K(0.5)) of 1 mM. Increasing [alphaMDG](o) also shifted the V(0.5) for Q and DeltaF to more positive values, with K(0.5)'s approximately 1 mM. The major difference between Q and DeltaF was that at saturating [alphaMDG](o), the presteady-state current (and Q(max)) was totally abolished, whereas DeltaF(max) was only reduced 50%. Phlorizin reduced both Q(max) and DeltaF(max) (K(i) approximately 0.4 microM), with no changes in V(0.5)'s or relaxation time constants. Simulations using an eight-state kinetic model indicate that external sugar increases the occupancy probability of inward-facing conformations at the expense of outward-facing conformations. The simulations predict, and we have observed experimentally, that presteady-state currents are blocked by saturating sugar, but not the changes in fluorescence. Thus we have isolated an electroneutral conformational change that has not been previously described. This rate-limiting step at maximal inward Na(+)/sugar cotransport (saturating voltage and external Na(+) and sugar concentrations) is the slow release of Na(+) from the internal surface of SGLT1. The high affinity blocker phlorizin locks the cotransporter in an inactive conformation.
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http://dx.doi.org/10.1085/jgp.200609643 | DOI Listing |
Clin J Am Soc Nephrol
January 2025
Post-graduate Program in Medical Sciences: Endocrinology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Int J Cardiol
January 2025
Department of Cardiology, Fujita Health University 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 4701192, Japan.
Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2is) reportedly decreased the new-onset atrial arrhythmias in patients with type-2 diabetes (T2DM) or heart failure (HF). This study examined the impact of SGLT2is on catheter ablation for atrial fibrillation (AF) in HF patients without T2DM.
Methods: Persistent AF (PeAF) and HF (N-terminal prohormone of brain natriuretic peptide, NT-proBNP ≥400 pg/ml) patients without T2DM undergoing catheter ablation were prospectively enrolled (n = 102).
Curr Issues Mol Biol
December 2024
Faculty of Veterinary Medicine, Ss. Cyril & Methodius University in Skopje, 1000 Skopje, North Macedonia.
The kidney plays an essential role in the proper homeostasis of glucose. In the kidney, glucose transport is carried out across cell membranes by two families of glucose transporters-facilitated diffusion glucose transporters (GLUTs) and Na(+)-dependent glucose co-transporters (SGLT family). Among the transporters, sodium-dependent glucose co-transporters play a major role in the kidney's ability to reabsorb glucose.
View Article and Find Full Text PDFDiabetes Metab J
December 2024
Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Center, Peking Union Medical College (PUMC), and Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, Beijing, China.
Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption.
View Article and Find Full Text PDFWorld J Clin Pediatr
December 2024
Department of Neonatal, The Second Affiliated Hospital of Xiamen Medical College, Xiamen 361021, Fujian Province, China.
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