Regulation of glucose transporters by insulin and extracellular glucose in C2C12 myotubes.

@article{Nedachi2006RegulationOG,
  title={Regulation of glucose transporters by insulin and extracellular glucose in C2C12 myotubes.},
  author={Taku Nedachi and Makoto Kanzaki},
  journal={American journal of physiology. Endocrinology and metabolism},
  year={2006},
  volume={291 4},
  pages={
          E817-28
        }
}
  • T. Nedachi, M. Kanzaki
  • Published 1 October 2006
  • Biology, Computer Science
  • American journal of physiology. Endocrinology and metabolism
It is well established that insulin stimulation of glucose uptake in skeletal muscle cells is mediated through translocation of GLUT4 from intracellular storage sites to the cell surface. However, the established skeletal muscle cell lines, with the exception of L6 myocytes, reportedly show minimal insulin-dependent glucose uptake and GLUT4 translocation. Using C(2)C(12) myocytes expressing exofacial-Myc-GLUT4-enhanced cyan fluorescent protein, we herein show that differentiated C(2)C(12… 
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References

SHOWING 1-10 OF 68 REFERENCES
C2C12 myocytes lack an insulin-responsive vesicular compartment despite dexamethasone-induced GLUT4 expression.
TLDR
The hypothesis that GLUT4 expression by itself is insufficient to establish an insulin-sensitive vesicular compartment is supported, as treatment of differentiating C2C12 myoblasts with dexamethasone causes a >or=10-fold increase in GLut4 expression but results in no significant change in insulin-stimulated glucose transport.
Acute Hyperglycemia Provides an Insulin-Independent Inducer for GLUT4 Translocation in C2C12 Myotubes and Rat Skeletal Muscle
TLDR
Glucose-induced GLUT4 translocation might represent an insulin-independent autoregulatory mechanism of the skeletal muscle to rapidly increase glucose uptake in acute hyperglycemia and Activation of PKC β might be involved in this mechanisum in skeletal muscle.
Differential expression of the GLUT1 and GLUT4 glucose transporters during differentiation of L6 muscle cells.
Expression of the glucose transporter isoform GLUT 4 is insufficient to confer insulin-regulatable hexose uptake to cultured muscle cells.
TLDR
The results suggest that acute insulin stimulation of glucose transport is not solely dependent on the presence of the insulin receptor and the GLUT 4 protein, and that the existence of some additional protein(s) must be required.
Glucose and Insulin Chronically Regulate Insulin Action via Different Mechanisms in BC3H1 Myocytes: Effects on Glucose Transporter Gene Expression
TLDR
The data generally support the idea that, in non-insulindependent diabetes mellitus, hyperglycemia and hyperinsulinemia can induce or exacerbate insulin resistance in target tissues.
Glucose transport in L6 myoblasts overexpressing GLUT1 and GLUT4.
TLDR
Both GLUT1 and GLUT4 can mediate insulin-stimulated glucose transport in L6 myoblasts, althoughGLUT4 is needed to observe large percentage increases comparable to those observed in skeletal muscle fibers in vivo, as well as in contrast to insulin, the protein phosphatase inhibitors, okadaic acid and calyculin A, inhibited glucose transport.
Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription.
Insulin and glucose-dependent regulation of the glucose transport system in the rat L6 skeletal muscle cell line.
Intracellular organization of insulin signaling and GLUT4 translocation.
TLDR
This chapter will focus on recently elucidated insulin signal transduction pathways andGLUT4 vesicle trafficking components that are necessary for insulin-stimulated glucose uptake and GLUT4 translocation in adipocytes.
Insulin-dependent protein trafficking in skeletal muscle cells.
TLDR
The normal level of GLUT-4 expression is not necessary for the structural organization and insulin-sensitive translocation of its cognate intracellular compartment and the sedimentation coefficient of these vesicles remains unchanged by denervation.
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