Glucose transport and cell surface GLUT-4 protein in skeletal muscle of the obese Zucker rat.

@article{Etgen1996GlucoseTA,
  title={Glucose transport and cell surface GLUT-4 protein in skeletal muscle of the obese Zucker rat.},
  author={G. Etgen and C. Wilson and J. Jensen and S. Cushman and J. Ivy},
  journal={The American journal of physiology},
  year={1996},
  volume={271 2 Pt 1},
  pages={
          E294-301
        }
}
The relationship between 3-O-methyl-D-glucose transport and 2-N-4-(1-azi-2,2,2-trifluoroethyl)-benzoyl-1, 3-bis-(D-mannos-4-yloxy)-2-propylamine (ATB-BMPA)-labeled cell surface GLUT-4 protein was assessed in fast-twitch (epitrochlearis) and slow-twitch (soleus) muscles of lean and obese (fa/fa) Zucker rats. In the absence of insulin, glucose transport as well as cell surface GLUT-4 protein was similar in both epitrochlearis and soleus muscles of lean and obese rats. In contrast, insulin… Expand
Epinephrine translocates GLUT-4 but inhibits insulin-stimulated glucose transport in rat muscle.
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  • Biology, Medicine
  • American journal of physiology. Endocrinology and metabolism
  • 1998
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It is indicated that epinephrine can translocate GLUT-4 while at the same time increasing glucose transport when insulin is absent, or can inhibit glucose transportWhen insulin is present. Expand
Epinephrine translocates GLUT-4 but inhibits insulin-stimulated glucose transport in rat muscle.
TLDR
It is indicated that epinephrine can translocate GLUT-4 while at the same time increasing glucose transport when insulin is absent, or can inhibit glucose transportWhen insulin is present. Expand
Effect of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside infusion on in vivo glucose and lipid metabolism in lean and obese Zucker rats.
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TLDR
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  • Chemistry, Medicine
  • American journal of physiology. Endocrinology and metabolism
  • 2006
TLDR
Chronic treatment of insulin-resistant, prediabetic obese Zucker rats with a specific GSK-3 inhibitor enhances oral glucose tolerance and whole body insulin sensitivity and is associated with an amelioration of dyslipidemia and an improvement in IRS-1-dependent insulin signaling in skeletal muscle. Expand
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Fatty acid transport proteins chronically relocate to the transverse-tubules in muscle from obese Zucker rats but are resistant to further insulin-induced translocation.
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FA transport proteins chronically relocate to the t-tubule domain in insulin resistant muscle, potentially contributing to lipid accumulation and to the accumulation of intramuscular lipids. Expand
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References

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Contraction stimulates translocation of glucose transporter GLUT4 in skeletal muscle through a mechanism distinct from that of insulin.
TLDR
Contraction-mediated translocation of the GLUT4 transporters to the cell surface was closely correlated with the glucose transport activity and could account fully for the increment in glucose uptake after contraction. Expand
Contraction-activated glucose uptake is normal in insulin-resistant muscle of the obese Zucker rat.
TLDR
The results suggest that maximal skeletal muscle glucose uptake of obese Zucker rats is resistant to stimulation by insulin but not to contractile activity and the relationship between contraction-stimulated glucose uptake and GLUT-4 content appears to be fiber-type specific. Expand
Glucose transport and GLUT4 protein distribution in skeletal muscle of GLUT4 transgenic mice.
TLDR
The results suggest that the increase in insulin-stimulated glucose transport following overexpression of the GLUT4 protein is limited by factors other than the plasma-membrane GLUT3 protein concentration, and is not coupled to glucose-metabolic capacity. Expand
Insulin resistance in obese Zucker rat (fa/fa) skeletal muscle is associated with a failure of glucose transporter translocation.
TLDR
It is concluded that the insulin resistance of the obese rats involves the failure of translocation of transporters, while the action of insulin to increase the average carrier turnover number is normal. Expand
The effects of muscle contraction and insulin on glucose-transporter translocation in rat skeletal muscle.
TLDR
Results suggest that insulin and muscle contraction are mobilizing two separate pools of GLUT-4 protein, and the increase in skeletal-muscle glucose uptake due to insulin + contraction is not due to an increase in plasma-membrane GLUT -4 protein concentration above that observed for insulin or contraction alone. Expand
Activation of glucose transport in diabetic muscle: responses to contraction and insulin.
TLDR
It appears that contractile activity can accelerate glucose transport in insulin-deficient muscle; however, the maximal capacity to activate glucose transport is decreased in skeletal muscle after sustained insulin deficiency. Expand
Skeletal muscle glucose transport in obese Zucker rats after exercise training.
TLDR
The results suggest that the improvement in the muscle insulin resistance of the obese Zucker rat after moderate endurance training was associated with an improved in the glucose transport process but that it was fiber-type specific. Expand
Effect of diffusion distance on measurement of rat skeletal muscle glucose transport in vitro.
TLDR
The results indicate that when muscles of different size and/or shape are used for in vitro measurement of glucose transport, the muscle preparations used must have similar diffusion distances for physiologically meaningful comparisons to be made. Expand
Glucose transport into rat skeletal muscle: interaction between exercise and insulin.
TLDR
Findings appear compatible with the hypothesis that the actions of exercise and insulin result in activation and/or translocation into the plasma membrane of two separate pools of glucose transporters in mammalian skeletal muscle. Expand
Exercise training, glucose transporters, and glucose transport in rat skeletal muscles.
TLDR
It is concluded that an increase inGLUT4, but not of GLUT1 protein, is a component of the adaptive response of muscle to endurance exercise and that the increase in GLUT4 protein is associated with an increased capacity for glucose transport. Expand
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