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The data presented in this article are related to the research article entitled “Regulation of GLUT4 activity in myotubes by 3-O-methyl-D-glucose” (Shamni et al., 2017) . These data show that the experimental procedures used to analyze the effects of 3-O-methyl-D-glucose (MeGlc) on the rate of hexose transport into myotubes were valid and controlled. The stimulatory effect of MeGlc was limited to glucose transporter 4 (GLUT4) and was independent of ambient glucose and protein synthesis. Cornish-Bowden kinetic analysis of uptake data revealed that MeGlc attenuated indinavir-induced inhibition of hexose transport in a competitive manner.
Value of the data
The data presented here are supportive to the data presented in  with no duplications or overlap. The data in Fig. 1 show that repetitive exposure of L6 myotubes to MeGlc augmented the rate of hexose transport into L6 myotubes that were maintained at 25 mM glucose. Fig. 2 shows that MeGlc stimulated hexose uptake in L6 myotubes maintained at 5 mM glucose and that these effects were similar to those observed under 25 mM glucose (Fig. 2 in ). No such stimulatory effects of MeGlc were evident in GLUT1 expressing vascular cells (Fig. 3). Analyses of [3H]MeGlc transport into wild-type L6 myotubes (Fig. 4) and of [3H] dGlc uptake into L6 myotubes expressing GLUT4myc (Fig. 5, Fig. 6) confirm the validity and suitability of the assays used. Inhibition of protein synthesis with cycloheximide did not interfere with MeGlc effects (Fig. 7). MeGlc exerted its effects also in the presence of glucose in the uptake assay (Fig. 8). Unlike MeGlc, its analog 1-α-methylglucose (1-α-MeGlc) failed to modulate the hexose transport system (Fig. 9). Finally, Cornish-Bowden analysis of the uptake data shows that MeGlc attenuated indinavir-induced inhibition of hexose transport in a competitive manner (Fig. 10).
Wild-type L6 myotubes, L6 myotubes expressing GLUT4myc and primary cultures of bovine aortic endothelial and smooth muscle cells were treated as described and then taken for standard [3H]dGlc uptake or [3H]MeGlc transport assays.
The authors would like to acknowledge support from the Hebrew University Applied Research Fund A (2011), the Baby Seed Fund of the Yissum Research Development Company of the Hebrew University of Jerusalem (2011), and the Alex Grass Center for Drug Design and Synthesis at the Hebrew University (2013). O.S. and G.C. received fellowships from the Hebrew University Center for Diabetes Research.
These data were used in part in the doctoral thesis Ofer Shamni submitted to the Senate of the Hebrew University of Jerusalem.
Transparency documentTransparency data document associated with this article can be found in the online version at http://dx.doi.org/10.1016/j.dib.2017.07.069.