Stimulation of Glucose Transport by Hypoxia: Signals and Mechanisms.

@article{Behrooz1999StimulationOG,
  title={Stimulation of Glucose Transport by Hypoxia: Signals and Mechanisms.},
  author={Alireza Behrooz and Faramarz Ismail-Beigi},
  journal={News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society},
  year={1999},
  volume={14},
  pages={
          105-110
        }
}
  • A. Behrooz, F. Ismail-Beigi
  • Published 1 June 1999
  • Biology
  • News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society
Glucose transport is acutely stimulated by hypoxia through enhanced GLUT-1 and GLUT-4 glucose transporter function. GLUT-1 expression is also stimulated by hypoxia or azide. Moreover, hypoxia per se, acting through hypoxia-inducible factor 1, enhances GLUT-1 transcription. GLUT-1 is the first gene whose transcription is dually stimulated in response to hypoxia and inhibition of oxidative phosphorylation. 

Figures from this paper

Hypoxic Regulation of Glucose Transport, Anaerobic Metabolism and Angiogenesis in Cancer: Novel Pathways and Targets for Anticancer Therapeutics
TLDR
Warburg’s original hypothesis is revisited and the recent clinical and basic research on the expression of GLUT family members in human cancers and in cell lines derived from human tumors are reviewed, exploring the links between hypoxia-induced genes, glucose transporters and angiogenic factors.
Glucose transporter 1 in health and disease
TLDR
This review mainly focuses on GLUT1 in physiological and pathological conditions and the recent advances related to its role in cancer development and applications in cancer therapeutics.
The regulation and importance of glucose uptake in the isolated Atlantic cod heart: rate-limiting steps and effects of hypoxia
TLDR
Activation of glucose transport is required to support hypoxic performance, the rate-limiting step for glucose utilization is glucose transport rather than glucose phosphorylation, 2-DG uptake accurately reflects glucose transport activity and glucose uptake in cod hearts does not involve an Na+-dependent mechanism.
The roles of hyperglycaemia and oxidative stress in the rise and collapse of the natural protective mechanism against vascular endothelial cell dysfunction in diabetes
TLDR
It is proved that pro-oxidants significantly increased the expression and plasma membrane abundance of GLUT-1 and the rate of glucose transport in VEC while abolishing high-glucose-induced down-regulation of the hexose transport system.
The effect of glucose on cardiac AMP-activated protein kinase
TLDR
The findings suggest that inactivation of AMPK by glucose may be mediated by the activity of the PPP which sets the level of Xu5P.
A Molecular and Whole Body Insight of the Mechanisms Surrounding Glucose Disposal and Insulin Resistance with Hypoxic Treatment in Skeletal Muscle
TLDR
The purpose of this review paper is to provide an insight into the mechanisms underpinning the observed effects and to open up discussions around the conflicting data surrounding hypoxia and glucose control.
Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway
TLDR
A pro-inflammatory stimulus like IL1β transforms excess glucose into a vascular deleterious agent by causing an increase in glucose uptake and its subsequent diversion into the PPP, promoting the pro-oxidant conditions required for the exacerbation of pro- oxidant and pro- inflammatory pathways.
A Primer on Carbohydrate Metabolism in the Heart
TLDR
Carbohydrate metabolism is a highly regulated, integral part of energy transfer and metabolic signaling in heart muscle and part of the nutrient signaling in the mTOR pathway.
Cholesterol Prevents Hypoxia-Induced Hypoglycemia by Regulation of a Metabolic Ketogenic Shift
TLDR
Results show for the first time that cholesterol contributes to metabolic shift and adaptation to hypoxia in vivo and in vitro through induction of HIF-1α and iNOS expression.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 21 REFERENCES
Dual Control of glut1 Glucose Transporter Gene Expression by Hypoxia and by Inhibition of Oxidative Phosphorylation*
TLDR
The results suggest that glut1 gene expression is regulated in a dual fashion by hypoxia per se and in response to inhibition of oxidative phosphorylation.
Hypoxia and Mitochondrial Inhibitors Regulate Expression of Glucose Transporter-1 via Distinct Cis-acting Sequences (*)
TLDR
Regulation of Glut-1 gene expression by hypoxia and mitochondrial inhibitors arises from the function of two different sensing systems, one of these responds to hypoxIA alone and resembles that involved in erythropoietin regulation, while the other responds to mitochondrial inhibitors and involves activation of a serum response element.
Enhancement of glucose transport in response to inhibition of oxidative metabolism: pre- and posttranslational mechanisms.
Addition of 5 mM sodium azide to Clone 9 cells, a rat liver cell line characterized by intracellular glucose concentrations of less than 10% that of the external medium and limited glycogen stores,
Glucose transporter expression in L6 muscle cells: regulation through insulin- and stress-activated pathways.
TLDR
The molecular mechanisms used by insulin and hypertonicity that culminate in the induction ofGLUT-1 and GLUT-3 are dissected and the mechanism(s) used by DNP remains unknown.
HIF-1, a Mediator of the Molecular Response to Hypoxia
ABSTRACT Normal oxygen delivery is essential for vertebrate homeostasis. Adaptation to changes in oxygen supply involves complex but specific changes in gene expression. This review summarizes rece...
Stabilization of vascular endothelial growth factor mRNA by hypoxia and hypoglycemia and coregulation with other ischemia-induced genes.
TLDR
Two different consequences of tissue ischemia, namely, hypoxia and glucose deprivation, induce VEGF and GLUT-1 expression by similar mechanisms, which function, in turn, to satisfy the tissue needs through expanding its vasculature and improving its glucose utilization, respectively.
Family of Glucose-Transporter Genes: Implications for Glucose Homeostasis and Diabetes
TLDR
A genetic defect resulting in reduced activity of this transporter could hypothetically lead to the two principal features of non-insulin-dependent diabetes mellitus, insulin resistance and relative hypoinsulinemia.
Induction of GLUT1 mRNA in response to inhibition of oxidative phosphorylation.
TLDR
This data indicates that suppression of oxidative phosphorylation in Clone 9 cells by 5 mM azide results in a marked biphasic stimulation of glucose transport that is mediated by GLUT1, and the mechanisms mediatingGLUT1 mRNA induction are investigated.
Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein.
TLDR
A model is proposed in which a ligand-dependent conformational change in a heme protein accounts for the mechanism by which hypoxia as well as cobalt and nickel stimulate the production of Epo.
...
1
2
3
...