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MeSH Review

Glycogenolysis

 
 
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Disease relevance of Glycogenolysis

 

Psychiatry related information on Glycogenolysis

 

High impact information on Glycogenolysis

  • The intracellular signal that links the cell-surface receptors for noradrenaline (alpha 1) and vasoactive peptides to activation of glycogenolysis is known to be a rise in the cytoplasmic concentration of free calcium ions (free Ca) [8].
  • Glycogenolysis induced by serotonin in brain: identification of a new class of receptor [9].
  • Although basal rates of glucose oxidation were reduced, insulin unexpectedly stimulated glucose oxidation and glycogenolysis in CIRKO hearts [10].
  • After overnight fasting, GP (fluxes in milligram per kilogram per minute) was 2.19+/-0.09, of which 0.79 (36%) was from gluconeogenesis, 1.40 was from glycogenolysis, 0.30 was retained in glycogen via UDP-gluconeogenesis, and 0.17 entered hepatic UDP-glucose by the direct pathway [11].
  • Preferential oxidation of glycogen may serve to ensure efficient generation of ATP from a limited supply of endogenous substrate, or as a mechanism to limit lactate accumulation during rapid glycogenolysis [12].
 

Chemical compound and disease context of Glycogenolysis

 

Biological context of Glycogenolysis

 

Anatomical context of Glycogenolysis

 

Associations of Glycogenolysis with chemical compounds

  • Therefore, in total insulin deficiency, MCR increases marginally with exercise (13% of normal); the beta adrenergic effects of catecholamines that stimulate both FFA mobilization and muscle glycogenolysis do not regulate muscle glucose uptake [28].
  • Equilibrations with water of the hydrogens bound to carbon 3 of pyruvate that become those bound to carbon 6 of glucose and of the hydrogen at carbon 2 of glucose produced via glycogenolysis are estimated from the enrichments to be approximately 80% complete [29].
  • The portion of the muscle glucose-6-phosphate (G6P) pool derived from net glycogenolysis was estimated from the ratio of specific activities of muscle UDPG and plasma glucose [18].
  • In contrast to anti-insulin serum, which produced marked elevations in plasma glucose, free fatty acid, and ketone body concentrations, glucagon treatment had little effect on any of these parameters, presumably due to enhanced insulin secretion after the initial stimulation of glycogenolysis [30].
  • Livers perfused with Krebs' Ringer bicarbonate buffer at normal (1.3 mL.g-1.min-1) and accelerated flow rates (3.0 mL.g-1.min-1) also showed a progressive decrease in bile flow and marked glycogenolysis as well as depletion of adenosine triphosphate content [31].
 

Gene context of Glycogenolysis

 

Analytical, diagnostic and therapeutic context of Glycogenolysis

References

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