Differential effects of glucose on dehydroascorbic acid transport and intracellular ascorbate accumulation in astrocytes and skeletal myocytes

Preincubation with sodium ascorbate potentiates insulin-dependent PKB/Akt and c-Jun phosphorylation in L6 rat myoblasts challenged with reactive oxygen/nitrogen species

“…Skeletal muscle and in L6 rat muscle cells in particular were reported to express GLUT-s (glucose transporters) or SVCT-s (sodium-vitamin C co-transporters) by several authors who studied the expression of these proteins and/or glucose/ascorbate transport (Korcok et al, 2003, Stuart et al, 2000, Taha et al, 1997. Taking into account the mechanisms that rule ascorbate/dehydroascorbate intracellular translocations one has to bear in mind rationale why sodium ascorbate has been chosen for our study.…”

“…Taking into account the mechanisms that rule ascorbate/dehydroascorbate intracellular translocations one has to bear in mind rationale why sodium ascorbate has been chosen for our study. The normal plasma concentration of AA is around 50-70 AM indicating that AA/DHA transporters should be responsible for the transport and accumulation of near milimolar concentration of vitamin C in skeletal muscles (Korcok et al, 2003).…”

Regulation of glucose transporters by insulin and extracellular glucose in C2C12myotubes

“…One possible explanation for this phenomenon is that a high level of basal glucose uptake, most likely mediated through GLUT1 (38), may mask insulin-induced augmentation of glucose uptake in response to GLUT4 translocation. In addition, numerous reports have shown that extracellular glucose concentrations during the preincubation period affect basal glucose transport activity (18,26,47,51,57). To examine this possibility, we examined the regulatory properties of glucose transport activity according to changes in extracellular glucose levels in G47-C 2 C 12 myotubes.…”

ATM and GLUT1-S490 Phosphorylation Regulate GLUT1 Mediated Transport in Skeletal Muscle

“…L6 myoblasts were serum starved for 3 hours, incubated in HEPES-Buffered Saline (HBS: 5 mM glucose, 20 mM HEPES, 140 mM NaCl, 5 mM KCl, 2.5 mM MgSO 4 , 1 mM CaCl 2 ) for 30 min in the presence or absence of ATM inhibitors/activators, washed several times with glucose-free HBS, and exposed to 2-deoxy-glucose (2DG) transport media (3 µCi/ml 3H-labeled 2DG, 10 µM 2DG, dissolved in glucose-free HBS) or DHA transport media (1 µCi/ml 14C-ascorbic acid, 2 U/ml ascorbate oxidase, and 200 µM DHA, dissolved in glucose-free HBS) [9] for 10 min. The cells were then washed with an ice-cold 0.9% saline solution, incubated with lysis buffer (0.2% SDS and 0.2 N NaOH) for 30 min, and processed for scintillation counting.…”

“…GLUT1 is reportedly responsible for about 30–40% of basal glucose uptake in skeletal muscle, with GLUT4 mediating the balance of basal glucose uptake [7], [8]. Furthermore, GLUT1 is a prominent transporter of dehydroascorbic acid (DHA) [9], [10], the oxidized form of ascorbic acid. GLUT3 and GLUT4 also display DHA transport activity, though the Km for DHA transport is higher for GLUT3 than it is for GLUT4 or GLUT1 [10], [11].…”