Insulin regulates the expression of the GLUT5 transporter in L6 skeletal muscle cells

@article{Hajduch2003InsulinRT,
  title={Insulin regulates the expression of the GLUT5 transporter in L6 skeletal muscle cells},
  author={{\'E}ric Hajduch and Gary J. Litherland and Sophie Turban and {\'E}dith Brot-Laroche and Harinder S. Hundal},
  journal={FEBS Letters},
  year={2003},
  volume={549}
}
Regulation of the fructose transporter GLUT5 in health and disease.
TLDR
This review describes the regulation of GLUT5 not only in the intestine and testis, but also in the kidney, skeletal muscle, fat tissue, and brain where increasing numbers of cell types have been found to haveGLUT5.
Fructose-induced ROS generation impairs glucose utilization in L6 skeletal muscle cells
TLDR
Exposure to fructose induces cell-autonomous oxidative response through ROS production leading to impaired insulin signaling and attenuated glucose utilization in skeletal muscle cells, which was prevented in the presence of antioxidants.
GLUT5-mediated fructose utilization drives lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling.
TLDR
It is demonstrated that, under the condition of coexistence of metabolic fuels in the body, fructose was readily used by LC cells in vivo as a glucose alternative via upregulating GLUT5, a major fructose transporter encoded by solute carrier family 2 member 5 (SLC2A5).
SLC2A5 promotes lung adenocarcinoma cell growth and metastasis by enhancing fructose utilization
TLDR
It is found that SLC2A5 is significantly upregulated in lung adenocarcinoma (LUAD) patients and overexpression of SLC5 is highly correlated with poor prognosis of LUAD patients and GLUT5 could be a potential target alone or combination with other treatment for lung cancer therapy.
Regulation of renal brush-border glucose transport in response to metabolic dysregulation
TLDR
Evidence is provided that GLUT2 expression at the proximal tubule BBM is not solely a response to hyperglycaemia but also a renal response to whole-body metabolic dysregulation, and the modulation of glucose transporters in models of metabolic syndrome associated with diabetes is elucidated.
Passive fructose transporters in disease: a molecular overview of their structural specificity.
TLDR
Although structure activity data has defined some aspects of fructose-specific uptake, a far more detailed clarification of the variables governing the onset and progression ofructose-correlated diseases is still needed.
Tissue-Specific Fructose Metabolism in Obesity and Diabetes
TLDR
An increase in sugar intake, particularly fructose, has been associated with the development of obesity and its complications, and inhibition of fructose utilization in tissues primary responsible for its metabolism alters consumption in other tissues, which have not been traditionally regarded as important depots of fructose metabolism.
Fructose fuels lung adenocarcinoma through GLUT5
TLDR
The required concentration for fructose to induce the peak effects on cell phenotype is significantly higher than that of glucose, indicating the differences in cellular uptaking and/or utilization of fructose or glucose, and fructose and glucose are differentially metabolized under in vitro experimental conditions.
Regulation of Skeletal Muscle Glucose Transport and Glucose Metabolism by Exercise Training
TLDR
The literature is reviewed and key gaps in current understanding of the effects of aerobic and resistance exercise training on the regulation of systemic glucose homeostasis, skeletal muscle glucose transport and skeletal Muscle glucose metabolism are highlighted.
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TLDR
The results indicate that the synergism between insulin and glucocorticoids on GLUT4 gene transcription is mediated throughGLUT4 promoter activation, and shows that insulin elicits an increase in GLut4 gene expression provided glucoc Corticoids are present.
Sustained exposure of L6 myotubes to high glucose and insulin decreases insulin-stimulated GLUT4 translocation but upregulates GLUT4 activity.
TLDR
It is shown that GLUT4 determines glucose uptake in L6 myotubes stably overexpressing myc-taggedGLUT4, and it is proposed that in a cellular model of skeletal muscle, chronic exposure to high Glc/Ins reduced the acute, insulin-elicited GLut4 translocation, resulting in a more robust glucose uptake than what would be predicted from the amount of cell surface GLUT 4 alone.
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TLDR
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TLDR
The present results show that GLUT5 is expressed in the sarcolemma of rat skeletal muscle and that it is likely to mediate fructose uptake in this tissue, and unlike the situation in absorptive and re-absorptive epithelia,GLUT5 expression in insulin-sensitive tissues is not regulated by increased substrate supply.
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TLDR
It is reported that rat adipocytes express the GLUT5 fructose transporter and that it is responsible for mediating a substantial component of the total cellular fructose uptake and that expression ofGLUT5 in rat adipocyte may be regulated by changes in blood glycaemia.
Glucose and thyroid hormone co-regulate the expression of the intestinal fructose transporter GLUT5.
TLDR
Electrophoretic-mobility-shift assays demonstrate that thyroid hormone receptors alpha and beta are expressed in Caco-2/TC7 cells and that the -308/-290 region of the GLUT5 promoter binds thyroid hormone receptor/retinoid X receptor heterodimers, and that glucose and/or T3 exert a deleterious effect on the binding of the nuclear protein complex.
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TLDR
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Human Small Intestine Facilitative Fructose/Glucose Transporter (GLUT5) Is Also Present in Insulin-Responsive Tissues and Brain: Investigation of Biochemical Characteristics and Translocation
TLDR
GLUT5 appears to be a constitutive sugar transporter that is expressed in many tissues and further studies are needed to define its overall contribution to fructose and glucose transport in insulin-responsive tissues and brain.
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