Nitric Oxide Stimulates Skeletal Muscle Glucose Transport Through a Calcium/Contraction– and Phosphatidylinositol-3-Kinase–Independent Pathway

@article{Etgen1997NitricOS,
  title={Nitric Oxide Stimulates Skeletal Muscle Glucose Transport Through a Calcium/Contraction– and Phosphatidylinositol-3-Kinase–Independent Pathway},
  author={G. Etgen and D. Fryburg and E. M. Gibbs},
  journal={Diabetes},
  year={1997},
  volume={46},
  pages={1915 - 1919}
}
Recently published data have provided evidence that nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) are signaling intermediates in the pathway through which muscle contraction stimulates glucose transport. As exercise promotes both NO production and calcium flux, we examined the relationships between NO-stimulated glucose uptake and calcium-, contraction-, and phosphatidylinositol-3-kinase (PI-3-K)-mediated glucose transport in the isolated incubated rat epitrochlearis muscle… Expand
Downstream mechanisms of nitric oxide-mediated skeletal muscle glucose uptake during contraction.
TLDR
Evidence is provided to suggest that NOS-derived oxidants regulate skeletal muscle glucose uptake during ex vivo contractions via a cGMP/PKG-, AMPK-, and p38 MAPK-independent pathway. Expand
Nitric oxide increases glucose uptake through a mechanism that is distinct from the insulin and contraction pathways in rat skeletal muscle.
TLDR
No stimulates glucose uptake through a mechanism that is distinct from both the insulin and contraction signaling pathways, suggesting that NO is a critical mediator of insulin- and/or contraction-stimulated transport. Expand
Evidence that Nitroprusside Stimulates Glucose Uptake in Isolated Rat Cardiomyocytes via Mitogen-activated Protein Kinase
TLDR
High SNP concentrations dose-dependently stimulate glucose uptake in cardiomyocytes and data suggest a role for MAPK signalling, but not PI-3-kinase and soluble guanylate cyclase, in stimulation of glucose uptake. Expand
Insulin Stimulates Glucose Transport Via Nitric Oxide/Cyclic GMP Pathway in Human Vascular Smooth Muscle Cells
TLDR
The results suggest that insulin-elicited glucose transport and the corresponding GLUT4 recruitment into the plasma membrane in human vascular smooth muscle cells is mediated by an increased synthesis of NO, which stimulates the production of cyclic GMP and the subsequent activation of a cyclicGMP–dependent protein kinase. Expand
Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes.
TLDR
No is capable of stimulating glucose transport through GLUT4 translocation in 3T3-L1 adipocytes, via a mechanism different from the insulin signaling pathway. Expand
Skeletal muscle glucose uptake during contraction is regulated by nitric oxide and ROS independently of AMPK.
TLDR
Testing the hypothesis that ROS and NO regulate skeletal muscle glucose uptake during contraction via an AMPK-independent mechanism found that they do so via interaction with AMP-activated protein kinase (AMPK), which is consistent with previous work on reactive oxygen species and nitric oxide. Expand
Results Insulin Stimulates Glucose Transport and a Rapid Increase of GLUT 4 at the Cell Surface in hVSMCs : Both Are
Objective—In cultured human vascular smooth muscle cells, insulin increases cyclic GMP production by inducing nitric oxide (NO) synthesis. The aim of the present study was to determine whether inExpand
Oxidative stress stimulates skeletal muscle glucose uptake through a phosphatidylinositol 3-kinase-dependent pathway.
TLDR
It is demonstrated that acute exposure of muscle to ROS is a potent stimulator of skeletal muscle glucose uptake and that this occurs through a PI3K-dependent mechanism. Expand
AMP kinase-induced skeletal muscle glucose but not long-chain fatty acid uptake is dependent on nitric oxide.
TLDR
The effects of AMP kinase (AMPK) activation on in vivo glucose and long-chain fatty acid (LCFA) uptake in skeletal muscle and the nitric oxide dependence of any putative effects are examined to show that the mechanisms by which AMPK stimulates glucose and LCFA uptake are distinct. Expand
Nitric oxide (NO) is involved in modulation of non-insulin mediated glucose transport in chicken skeletal muscles.
  • Y. Nishiki, T. Kono, +4 authors Y. Akiba
  • Chemistry, Medicine
  • Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
  • 2008
TLDR
The results suggest that NO plays a lesser role in the modulation of glucose transport in chicken skeletal muscle compared to mammals and may be involved in non-insulin mediated glucose transport. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 19 REFERENCES
Evidence that nitric oxide increases glucose transport in skeletal muscle.
TLDR
The results suggest that NO may be a potential mediator of exercise-induced glucose transport, and chronic treadmill training increased protein expression of both type I and type III NOS in soleus muscle homogenates. Expand
Calcium stimulates glucose transport in skeletal muscle by a pathway independent of contraction.
TLDR
Evidence is provided suggesting that an increase in cytoplasmic Ca2+ too low to cause contraction or [approximately P] depletion can bring about a increase in glucose transport activity in skeletal muscle. Expand
Nitric oxide stimulates glucose transport and metabolism in rat skeletal muscle in vitro.
TLDR
Nitric oxide (from SNP or spermine NONOate) increases the rate of glucose transport and metabolism, an effect independent of insulin and SNP stimulates cGMP formation, which mediates, at least partly, the effects on glucose metabolism; nitric oxide-mediated stimulation of glucose utilization might occur in fibre contraction. Expand
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
Nitric oxide release is present from incubated skeletal muscle preparations.
TLDR
The data indicate that NO is released from an incubated skeletal muscle preparation and presents the possibility that muscle-derived NO may play an important metabolic role and reduce both basal 2-deoxyglucose transport and NO efflux. Expand
The Effects of Wortmannin on Rat Skeletal Muscle
TLDR
Results support the view that PI 3-kinase is involved in the signaling pathways mediating insulin-responsive glucose transport in skeletal muscle but is not required for stimulation by hypoxia or contraction and indicate that there exist at least two signaling pathways leading to activation of glucose Transport in skeletal Muscle with differential sensitivities to wortmannin. Expand
Nitric oxide in skeletal muscle
TLDR
It is shown that rat skeletal muscle expresses neuronal-type NO synthase and that activity varies among several respiratory and limb muscles, and that two physiological functions of NO in skeletal muscle are supported. Expand
Exercise training reverses insulin resistance in muscle by enhanced recruitment of GLUT-4 to the cell surface.
TLDR
Training improves insulin-stimulated glucose transport in muscle of the obese Zucker rat by increasing GLUT-4 content and by altering the normal intracellular distribution of these transporters such that they are now capable of migrating to the cell surface in response to the insulin stimulus. Expand
Interactions between effects of W-7, insulin, and hypoxia on glucose transport in skeletal muscle.
TLDR
Detailed interactions between the effects of W-7 and those of hypoxia and of insulin on glucose transport demonstrate that W- 7 selectively inhibits insulin stimulation of glucose transport. Expand
Glucose transport and cell surface GLUT-4 protein in skeletal muscle of the obese Zucker rat.
TLDR
The reduced glucose transport response to insulin in skeletal muscle of the obese Zucker rat appears to result directly from an inability to effectively enhance cell surface GLUT-4 protein. Expand
...
1
2
...