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Glycogenolysis inhibition

Phosphoglucomutase Involved in glycogenolysis inhibition by lithium of unknown relevance... [Pg.639]

Glucose-Metabolism Stimulation of cellular glucose uptake Inhibition of glycogenolysis Inhibition of gluconeogenesis... [Pg.159]

Not only is phosphorylase activated by a rise in concentration of cAMP (via phosphorylase kinase), but glycogen synthase is at the same time converted to the inactive form both effects are mediated via cAMP-dependent protein kinase. Thus, inhibition of glycogenolysis enhances net glycogenesis, and inhibition of glycogenesis enhances net glycogenolysis. Furthermore,... [Pg.150]

Figure 18-8. Coordinated control of glycogenolysis and glycogenesis by cAMP-dependent protein kinase. The reactions that lead to glycogenolysis as a result of an increase in cAMP concentrations are shown with bold arrows, and those that are inhibited by activation of protein phosphatase-1 are shown as broken arrows. The reverse occurs when cAMP concentrations decrease as a result of phosphodiesterase activity, leading to glycogenesis. Figure 18-8. Coordinated control of glycogenolysis and glycogenesis by cAMP-dependent protein kinase. The reactions that lead to glycogenolysis as a result of an increase in cAMP concentrations are shown with bold arrows, and those that are inhibited by activation of protein phosphatase-1 are shown as broken arrows. The reverse occurs when cAMP concentrations decrease as a result of phosphodiesterase activity, leading to glycogenesis.
Glycogen phosphorylase isoenzymes have been isolated from liver, brain and skeletal muscle. All forms are subject to covalent control with conversion of the inactive forms (GP-b) to the active forms (GP-a) by phosphorylation on specific serine residues. This phosphorylation step, mediated by the enzyme phosphorylase kinase, is initiated by glucagon stimulation of the hepatocyte. Indeed, the same cAMP cascade which inhibits glycogen synthesis simultaneously stimulates glycogenolysis, giving us an excellent example of reciprocal control. [Pg.213]

Answer C. Insulin increases glucose transport in only two tissues, adipose and muscle. The major site of glucose uptake is muscle, which decreases hyperglycemia. Glucose and ketone transport and metabolism are insulin independent in the brain (choice D). Insulin would slow gluconeogenesis (choice A) and fatty acid release from adipose (choice B). Insulin would inhibit glycogenolysis in the liver (choice E). [Pg.160]

Glycogen deposits in the liver (glucose 6-P stimulates glycogen synthesis, and glycogenolysis is inhibited)... [Pg.195]

In addition to inhibition of glycogenolysis, glucose also activates glycogen synthase and hence stimulates glycogen synthesis and this is achieved by an even more intriguing... [Pg.120]

Insulin inhibits glycogenolysis and gluconeogenesis. Glucagon opposes the effects of insulin and therefore helps to maintain the blood glucose level so that it has the same end result as that of fatty acid oxidation (See Figure 12.14). [Pg.366]

L. Nprskov-Lauritsen, and L. Agius, Iminosugars as potential inhibitors of glycogenolysis Structural insights into the molecular basis of glycogen phosphorylase inhibition,./. Med. Chem., 49 (2006) 5687-5701. [Pg.293]

The decreased insulin/glucagon ratio leads to inhibition of glycogen synthesis and increased glycogenolysis to supply some of the body s glucose needs on an immediate basis. [Pg.62]

Sulfonylureas inhibit neoglucogenesis and glycogenolysis. Sulfonylureas are rapidly absorbed from the gastrointestinal tract after oral administration and are more than 90 percent bound to plasma proteins and excreted unchanged in urine. [Pg.278]

Activation of Gs or Gi proteins results in stimulation or inhibition, respectively, of adenylyl cyclase which catalyses the formation of cyclic adenosine monophosphate (cAMP) from ATP The cAMP binds to protein kinase A (PKA), which mediates the diverse cellular effects of cAMP by phosphorylating substrate enzymes, thereby increasing their activity. Among the responses mediated by cAMP are increases in contraction of cardiac and skeletal muscle and glycogenolysis in the liver by adrenaline (epinephrine). Because a single activated receptor can cause the conversion of up to 100 inactive Gs proteins to the active form, and each of these results in the synthesis of several hundred cAMP molecules, there is a very considerable signal amplification. For example, adrenaline concentrations as low as 10-10 M can stimulate the release of glucose sufficient to increase... [Pg.24]


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Glycogenolysis

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