Corticosterone Impairs Insulin-Stimulated Translocation of GLUT4 in the Rat Hippocampus

@article{Piroli2007CorticosteroneII,
  title={Corticosterone Impairs Insulin-Stimulated Translocation of GLUT4 in the Rat Hippocampus},
  author={Gerardo G. Piroli and Claudia A. Grillo and Leah R Reznikov and Sheila M. Adams and Bruce S. McEwen and Maureen J. Charron and Lawrence P. Reagan},
  journal={Neuroendocrinology},
  year={2007},
  volume={85},
  pages={71 - 80}
}
Background: Exposure to stress levels of glucocorticoids produces physiological responses that are characteristic of type 2 diabetes, such as peripheral insulin resistance and impairment in insulin-stimulated trafficking of glucose transporter 4 (GLUT4) in muscle and fat. In the central nervous system, stress produces neuroanatomical and neurochemical changes in the hippocampus that are associated with cognitive impairments. Methods: In view of these observations, the current studies examined… 
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References

SHOWING 1-10 OF 80 REFERENCES
GLUT4 glucose transporter expression in rodent brain: effect of diabetes
TLDR
A chronic insulin-sensitive regulation of GLUT4 in rodent brain is demonstrated and the possibility of acute modulations of glucose uptake in these GLUT1 and GLUT3 expressing cells is raised.
Role of Glucose Transporters in Glucocorticoid-Induced Insulin Resistance: GLUT4 Isoform in Rat Skeletal Muscle is Not Decreased by Dexamethasone
TLDR
It is concluded that glucocorticoid-induced insulin resistance in skeletal muscle is not due to suppression of glucose transporter gene expression and that GLUT4 protein concentration in soleus and extensor digitorum longus extracts was not significantly increased by dexamethasone treatment.
Effects of glucocorticoid excess on the sensitivity of glucose transport and metabolism to insulin in rat skeletal muscle.
TLDR
A redistribution of glucose away from the pathway of glycogen synthesis and glucose oxidation could maintain a normal rate of lactate formation although the rate of glucose transport is decreased, and the changes in the sensitivity of glucose phosphorylation to insulin seen under these conditions are secondary to those in glucose transport.
Glucocorticoid regulation of insulin receptor and substrate IRS-1 tyrosine phosphorylation in rat skeletal muscle in vivo.
TLDR
Glucocorticoid-induced hyperinsulinemia appears to be essential for the development of these alterations in insulin receptor signaling, and a reduction in the pool of receptors undergoing tyrosine phosphorylation of IRS-1 is characterized.
Expression and localization of insulin-regulatable glucose transporter (GLUT4) in rat brain
TLDR
The results suggest that insulin-sensitive glucose uptake may occur in some specific cells of the brain but is regulated in a different manner from those in peripheral cells.
Glucocorticoid-Induced Insulin Resistance: Dexamethasone Inhibits the Activation of Glucose Transport in Rat Skeletal Muscle by Both Insulin- and Non-Insulin-Related Stimuli
TLDR
Dex treatment reduces basal glucose transport and decreases the maximal response of skeletal muscle glucose transport to insulin, the related hormone IGF-I, and the non-insulin-related stimulus hypoxia, support the hypothesis that glucocorticoids may also act by inhibiting the glucose transport system, per se.
In vivo effects of dexamethasone and sucrose on glucose transport (GLUT-4) protein tissue distribution.
TLDR
The results emphasize the specific regulation of GLUT-4 in insulin-sensitive tissues as well as the importance of dexamethasone administration in this area.
Dexamethasone inhibits insulin-stimulated recruitment of GLUT4 to the cell surface in rat skeletal muscle.
TLDR
Findings indicate that glucocorticoid-induced inhibition of insulin-stimulated glucose transport in muscle is due to impaired recruitment of GLUT4 to the cell surface.
Peripheral glucose administration stimulates the translocation of GLUT8 glucose transporter to the endoplasmic reticulum in the rat hippocampus
TLDR
It is demonstrated that GLUT8 undergoes rapid translocation to the rough ER in the rat hippocampus following peripheral glucose administration, trafficking that is impaired in STZ diabetes, suggesting that insulin serves as a stimulus forGLUT8 translocation in hippocampal neurons.
Oxidative stress and HNE conjugation of GLUT3 are increased in the hippocampus of diabetic rats subjected to stress
TLDR
The results demonstrate that the hippocampus is vulnerable to increases in oxidative stress produced by diabetes and stress, and increases in HNE protein conjugation of GLUT3 provide a potential mechanism for stress- and diabetes-mediated decreases in hippocampal neuronal glucose utilization.
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