Endothelin Stimulates Glucose Uptake and GLUT4 Translocation via Activation of Endothelin ETA Receptor in 3T3-L1 Adipocytes*

@article{Wuwong1999EndothelinSG,
  title={Endothelin Stimulates Glucose Uptake and GLUT4 Translocation via Activation of Endothelin ETA Receptor in 3T3-L1 Adipocytes*},
  author={J. R. Wu-wong and C. Berg and J. Wang and W. Chiou and B. Fissel},
  journal={The Journal of Biological Chemistry},
  year={1999},
  volume={274},
  pages={8103 - 8110}
}
Endothelin-1 (ET-1) is a 21-amino acid peptide that binds to G-protein-coupled receptors to evoke biological responses. This report studies the effect of ET-1 on regulating glucose transport in 3T3-L1 adipocytes. ET-1, but not angiotensin II, stimulated glucose uptake in a dose-dependent manner with an EC50 value of 0.29 nm and a 2.47-fold stimulation at 100 nm. ET-1 stimulated glucose uptake in differentiated 3T3-L1 cells but had no effect in undifferentiated cells, although ET-1 stimulated… Expand
Endothelin stimulates glucose uptake via activation of endothelin-A receptor in neonatal rat cardiomyocytes.
TLDR
The results show that ET-1 stimulates glucose uptake in neonatal rat cardiomyocytes via activation of the ET(A)-receptor through stimulation of the extracellular signal-regulated kinase (ERK1/2). Expand
Endothelin-1 increases glucose transporter glut1 mRNA accumulation in 3T3-L1 adipocytes by a mitogen-activated protein kinase-dependent pathway.
TLDR
Results suggest that ET-1 may induce GLUT1 gene expression by a MAPK-dependent mechanism. Expand
Endothelin-1-stimulated glucose uptake is desensitized by tumor necrosis factor-alpha in 3T3-L1 adipocytes.
  • N. Rachdaoui, L. Nagy
  • Biology, Medicine
  • American journal of physiology. Endocrinology and metabolism
  • 2003
TLDR
It is suggested that TNF-alpha-induced desensitization of endothelin-1-stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes is due, at least in part, to a decreased expression of Galphaq/11, leading to a suppression in tyrosine phosphorylation of PYK2. Expand
The acute and chronic stimulatory effects of endothelin-1 on glucose transport are mediated by distinct pathways in 3T3-L1 adipocytes.
TLDR
The findings suggest that ET-1 induced GLUT1 protein expression is primarily mediated via MAPK, and partially via PI3K in 3T3-L1 adipocytes. Expand
Endothelin-stimulated glucose uptake: effects of intracellular Ca(2+), cAMP and glucosamine.
TLDR
The results suggest that ET-1-induced glucose uptake is independent of its effects on modulating intracellular Ca(2+) and cAMP levels, but is likely linked to the hexosamine biosynthetic pathway. Expand
Endothelin-1-induced GLUT4 Translocation Is Mediated via Gαq/11 Protein and Phosphatidylinositol 3-Kinase in 3T3-L1 Adipocytes*
TLDR
It is found that Gαq/11 formed immunocomplexes with the type-A endothelin receptor and the 110α subunit of PI 3-kinase and that ET-1 stimulation enhances tyrosine phosphorylation of Gβγ/11. Expand
The Acute and Chronic Stimulatory Effects of Endothelin-1 on Glucose Transport Are Mediated by Distinct Pathways in 3T3-L1 Adipocytes* *This work was supported by NIH Grant DK-33651.
TLDR
Another pathway by which ET-1 potentiates glucose transport in 3T3-L1 adipocytes is presented, which was almost completely blocked by the protein-synthesis inhibitor, cycloheximide and the RNA-symbolic inhibitor, actinomycin... Expand
ADP-Ribosylation Factor 6 Delineates Separate Pathways Used by Endothelin 1 and Insulin for Stimulating Glucose Uptake in 3T3-L1 Adipocytes
TLDR
Endothelin stimulates glucose transport through a pathway that is distinct from that utilized by insulin but is likely to depend on both a heterotrimeric G protein from the Gq family and the small G protein ARF6, consistent with the interpretation that endothelin and insulin stimulate functionally different pools of glucose transporters to be redistributed to the plasma membrane. Expand
Synergistic effect of endothelin-1 and cyclic AMP on glucose transport in 3T3-L1 adipocytes.
TLDR
Results indicate that ET-1 may act with cAMP in a synergistic way to increase glucose transport, probably through enhanced GLUT1 expression via a PKC-dependent mechanism. Expand
Endothelin-1 induces lipolysis in 3T3-L1 adipocytes.
TLDR
The data show that ET-1 induces lipolysis in 3T3-L1 adipocytes via a pathway that is different from the conventional cAMP-dependent pathway used by isoproterenol and that involves ERK activation. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 36 REFERENCES
Gq-coupled Receptors Transmit the Signal for GLUT4 Translocation via an Insulin-independent Pathway*
TLDR
Evidence is obtained that the activation of receptor-coupled Gq (neither Gi nor Gs) triggeredGLUT4 translocation in cells, independently of insulin signaling pathway(s), which may possibly contribute to the fuel supply required for thermogenesis in brown adipocytes and for the enhanced contractility in cardiomyocytes, both of which have an abundant endogenous GLUT4. Expand
Effects of wortmannin on increased glucose transport by insulin and norepinephrine in primary culture of brown adipocytes.
TLDR
Results indicate that PI 3-kinase plays a critical role on insulin-induced translocation of GLUT4, but that this pathway is not involved in the increase in glucose transport by NE in brown adipocytes. Expand
Endothelin and isoproterenol counter-regulate cAMP and mitogen-activated protein kinases.
TLDR
It is suggested that counter-regulation among various ligands and cross-talk among different signaling pathways may be required to modulate biologic functions in a living cell. Expand
Endothelin receptors in human smooth muscle cells: antagonist potency differs on agonist-evoked responses.
TLDR
Endothelin (ET) receptors in human pericardium smooth muscle cells (HPSMC) are characterized and the potency of antagonists on ET-evoked signal transduction and DNA synthesis is examined. Expand
Endothelin-1-evoked arachidonic acid release: a Ca(2+)-dependent pathway.
TLDR
The data suggest that the effect of ET on AA release in HPSMC is via phospholipase A2, which is modulated by Ca2+ and PKC, which means that ET-1-evoked AA release closely followed the change in the intracellularCa2+ concentration. Expand
Endothelin-1 induces insulin resistance in conscious rats.
TLDR
Results unequivocally indicated that intraperitoneally administered ET-1 induces insulin resistance in conscious rats. Expand
Insulin and nonhydrolyzable GTP analogs induce translocation of GLUT 4 to the plasma membrane in alpha-toxin-permeabilized rat adipose cells.
TLDR
Rat adipose cells treated with Staphylococcus aureus alpha-toxin are permeable and retain their ability to respond to insulin after hormone treatment, suggesting the involvement of a GTP-binding protein in insulin-triggered recruitment of GLUT 4 to the cell surface. Expand
NG-methyl-L-arginine and somatostatin decrease glucose and insulin and block endothelin-1 (ET-1)-induced insulin release but not ET-1-induced hypoglycemia.
TLDR
The present study confirms the previous finding that endothelin-1 decreases blood glucose and increases plasma insulin and suggests that ET-1-induced insulin release may be mediated by production of nitric oxide. Expand
Increased GLUT-4 translocation mediates enhanced insulin sensitivity of muscle glucose transport after exercise.
TLDR
It is concluded that the increase in muscle insulin sensitivity of glucose transport after exercise is due to translocation of more GLUT-4 to the cell surface and that this effect is not due to potentiation of insulin-stimulated tyrosine phosphorylation. Expand
G-protein-mediated regulation of the insulin-responsive glucose transporter in isolated cardiac myocytes.
TLDR
A functional association between the insulin-responsive glucose transporter and a cholera-toxin-sensitive G-protein mediating stimulation by insulin and isoprenaline is suggested. Expand
...
1
2
3
4
...